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LELAND  STANFORD  JUNIOR  UNIVERSITY  PUBLICATIONS 
UNIVERSITY  SERIES 


TheJPathology  of  Nephritis 

as  illustrated  by  thirty-two  consecutive  cases 


BY 


WILLIAM  [OPHULS 

Professor  of  Pathology 


From  the  Division  of  Pathology 
Stanford  University  Medical  School 


STANFORD  UNIVERSITY,  CALIFORNIA 

PUBLISHED  BY  THE  UNIVERSITY 

1916 


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571ti 


LELAND  STANFORi:)  JUNIOR   UNIVHRSITY  PUBLICATIONS 
UNIVHRSITV  SHRIES 


The  Pathology  of  Nephritis 

as  illustrated  bv  thirtN'-two  consecutive  cases 


WILLIAM  OfHULS 

Professor  of  Pathology 


From  tlie  Division  of  Pathology 
Stanford  University  Medical  School 


STANFORD  UN'IVERSITY,  CALIFORNIA 

PUBLISHED  BY  THE   UNIVERSITY 

1916 


Stanford   University 
Pkess 


353 


TO  ALL  THOSE  WHO  CONTRIBUTED 
IN  THE  COLLECTION  OF  THE  CLIN- 
ICAL DATA  UTILIZED  RY  THE  AUTHOR 


7n(;n^D 


THE  PATHOLOGY  OF  NHPHRIUS 

AS  II.I.DSTRATED  BY 
miR  I'lTWO   CONSECUTIVE   CASES 

It  may  seem  ]iresum|ilii(iii>  mi  the  ipatt  cil'  a  |)alli()Iii,i;i>t  to  atlempl 
to  write  a  treatise  on  the  I'atholoj^y  of  W-iili litis  inchi(lin|L;-  a  resume  of 
tlie  symptomatology  of  the  disease,  hecause  the  evidence  collected  from 
the  histories  of  tlie  patients  i^  necessarily  second-hand  and  incomjilete 
and  the  author  i>  not  iraiiud  in  the  interpretation  and  evaluation  of 
clinical  phenomena.  It  may  Ijc  coiiteiuled.  however,  that  the  careful 
judicious  contemplation  of  a  clinical  liistory  liy  some  one  not  connected 
with  the  case  and  not  interested  in  the  matter  of  clinical  diaifnosis — 
])rovided  he  has  the  necessary  knowledge  of  .Medicine  in  general — may 
bring  out  the  salient  points  in  the  biology  of  the  disease  with  greater 
clearness.  1  lowever  that  may  be.  since  it  became  necessary  to  consult 
the  records  in  trying  to  solve  the  etiological  (|iiestions  involved,  an  at- 
tempt has  been  made  to  give  an  outline  of  the  progress  of  the  disease  in 
each  individual  case  as  brielly  as  i)ossible.  without  entering  into  aii\  of 
the  many  details  that  are  chiefly  of  clinical  importance. 

The  aim  has  been  to  collect  in  each  case  all  relevant  data  which 
migiit  have  any  bearing  on  the  etiology,  progress  and  termination  of  the 
disease.'  To  this  was  added  an  abstract  of  all  autoi)sy  findings  which 
might  be  of  interest,  and  an  esjjecially  careful  descri])tion  of  the  findings 
in  the  kidneys,  both  in  the  gross  and  microscopically.  Since  no  mere 
descri])tion  in  words  can  convey  an  adec|uale  conception  of  the  fmdings. 
photograjihs  of  the  gross  specimens  have  been  added  wherever  feasible, 
and  in  all  cases  photomicrograjihs  of  the  diseased  kidneys.  The  latter, 
of  course,  reproduce  only  a  very  small  area  of  the  tissues  e.xamined  ; 
but  an  attempt   has  been   made   to   show    as   much   as   ])ossible   without 


•  The  results  of  functional  tests  li.ivc  not  hci-n  considered,  vvilli  the  exception 
(jf  an  occasional  reference  to  the  phenolsulphone-plitlialein  lest.  'I  his  has  been 
done,  not  because  their  great  scientilic  interest  and  practical  value  is  not  fully 
recognized,  but  because  many  cases  antedated  the  use  of  such  functional  tests,  so 
that  the  evidence  in  the  few  recent  cases  is  hardly  sufticieiit  to  warr.uit  any  <leduc- 
tions.  .\n  attempt  to  go  into  this  question,  in  vvhicli  all  clinical  workers  at  present 
are  deeply  interested,  would  also  h.ive  i>pened  up  such  a  large  field  for  <liscHssion 
that  it  seemed  wise  to  refrain  from  discussing  it  altogether. 


6  Tin-:  i'ATii()i.()(;v  of  nkimiritis 

losing  all  detail,  and  lo  select  for  rcjirodiiction  as  representative  ]ilaccs 
as  possible  in  the  sections.  The  tissues  were  hardened  in  ()rth"s  mix- 
ture and  stained  with  haematoxylin-eosin,  or  according  to  van  Gieson's 
method.  In  each  case  several  sections  were  also  stained  with  W'eigert's 
stain  for  elastic  fibers,  and  with  Giemsa's  stain  for  bacteria,  and  in  order 
to  bring  out  the  characteristic  granulations  of  the  various  leucocytes. 

All  photographs  and  photomicrographs  are  comparable  with  one 
another,  since  all  jjhotograi^hs  have  been  taken  at  about  one-half  normal 
size,  and  all  photomicrographs  at  the  same  magnification  (  ^~  times  nat- 
ural size). 

It  is  hoped  that  the  cases  as  represented  will  s[)eak  for  themselves. 
The  comments  which  precede  them  serve  the  [)urpose  of  presenting  some 
of  the  main  facts  in  a  readable  manner,  and  also  to  draw  such  conclu- 
sions from  them  as  may  seem  warranted. 

The  cases,  in  the  opinion  of  the  author,  are  all  cases  of  true  iliffuse 
glomerulo-nephritis,  and  represent  all  such  cases  that  were  encountered 
in  a  consecutive  series  of  about  nine  himdred  necropsies.  They  are  the 
same  cases  which  were  used  in  i)rei)aring  the  author's  previous  publica- 
tion in  the  Journal  of  the  American  Medical  Association  in  1915.  where 
a  summary  of  the  findings  is  given  under  the  headings  of  acute,  subacute, 
and  chronic  glomerulo-nephritis.  It  is  unlikely  that  any  case  of  import- 
ance escaped  detection,  because  microscopic  sections  of  the  kidneys  were 
examined  in  all  nine  hundred  cases,  and  in  the  vast  majority  of  instances 
personally  by  the  writer.  All  cases  of  chronic  parenchymatous  nephritis 
with  amyloid  disease  have  been  excluded,  as  also  all  cases  in  which  the 
renal  lesions  were  evidently  of  minor  im])ortance  as  compared  with  co- 
existing arterial  disease. 

For  convenience'  sake  the  main  data  of  each  case  have  been  gathered 
in  one  large  table,  which  is  placed  at  the  end  of  the  volume. 

A  historical  review  of  the  subject  is  purposely  omitted,  because  to 
cover  this  part  of  the  subject  adequately  would  consume  much  space — 
unnecessarily,  it  would  seem,  because  the  subject  has  been  dealt  with  ex- 
tensively and  adequately  by  other  writers.  Since  the  author  has  pre- 
viously attempted  to  present  what  api)eared  to  him  the  main  facts  in  the 
historical  development  of  the  subject,  and  has  attempted  to  give  due 
credit  for  previous  work,  he  hopes  to  escape  the  imputation  that  he 
attempts  to  assume  more  credit  than  is  due  for  his  own  efforts.  In  fact, 
the  author  specifically  disclaims  all  credit  to  himself  except  that  which 
may  be  due  to  the  careful  presentation  of  a  series  of  case-reports.  His 
comments  are  merely  expressions  of  his  personal  opinion,  and  are  based, 
naturally,  not  only  on  his  own  observations,  but  upon  the  splendid  work 


INIKlllHl   TION  7 

done  liy  luimerdiis   invostiiiators   rcccntlv    and  diirinL;   llio  course  of  the 
last  century. 

Since  in  teacliini;  it  is  necessary  always  to  i;o  hack  to  tiie  sources  of 
orif.;inal  information,  a  series  of  com|)lete  case-re])orts  of  one  particular 
disease  should  be  of  ^;reat  benefit  to  teacher  and  student.  It  would 
be  especially  ijratifyinsj  to  the  author  if  thi>  little  xohinie  should  jirove 
to  be  useful  for  teacliin_a;  purposes. 


THE    I'ATIIOI.OCV    Ul-    NHI'IIKITIS 


I.  Acute  Glomerulo-Xephritis   (Cases   1-4). 

The  first  two  patients  were  males  of  over  50  years  of  age.  with  old 
infectious  endocarditis  of  the  aortic  orifice.  According  to  the  histories, 
and  also  according  to  the  anatomical  findings,  the  original  infection 
dated  back  many  years ;  in  the  first  case,  at  least  eight,  and  in  the  second 
altogether  twenty  years.  The  course  of  the  disease  in  both  cases  was 
quite  the  usual  one  for  chronic  endocarditis,  and  the  patients  died  in  one 
of  the  exacerbations. 

The  nephritis  in  both  cases  was  terminal  and  incidental  to  the  main 
disease.  In  the  first  case  it  revealed  itself  clinically  by  \ery  definite 
urinary  findings,  and  by  a  slowing  of  the  phenolsulphone-phthalein  secre- 
tion. In  the  second  case  the  urinary  changes  were  very  slight — so  much 
so  that  the  condition  might  very  well  have  been  overlooked  clinically. 

In  both  cases  diplostreptococci  were  found  in  the  lesions  in  the 
heart  valves,  and  in  the  first  case  also  in  the  urine,  and  in  the  spleen  at 
necropsy. 

The  kidneys  in  these  two  cases  were  not  as  yet  very  much  swollen  : 
the  cortex  was  somewhat  opaque,  the  seat  of  petechial  haemorrhages. 
The  glomeruli  showed  the  very  earliest  lesions:  hyaline  necroses  of  some 
of  the  loops,  and  a  very  marked  infiltration  with  neutrophilic  leucocytes. 
In  case  2  there  was  some  extra-capillary  proliferation  in  the  glomeruli, 
and  a  slight  infiltration  of  the  adjoining  connecti\e  tissue  with  neutro- 
philic leucocytes.  There  had  been  much  bleeding  irom  the  diseased 
glomeruli,  and  also  escape  of  some  leucocytes  into  the  tubules.  There 
were  as  yet  few  casts,  and  the  epithelium  was  nearly  unaltered. 

In  the  case  (  i  )  in  which  the  bacteria  were  found  in  the  urine,  no 
bacteria  were  found  in  sections  of  the  kidneys  either  in  the  glomeruli  or 
in  the  tubules ;  but  there  were  many  capillary  diplostreptococcic  emboli 
between  the  tubules,  some  with  beginning  suppuration  about  them.  This 
is  one  of  the  cases  which  so  strongly  suggest  that  in  glomerulo-nephritis 
coccus  embolism  does  take  place  in  the  glomeruli,  but  that  in  these  struc- 
tures the  bacteria  are  rapidly  dissolved,  in  this  way  causing  the  hyaline 
thrombosis  and  necrosis  of  the  vascular  loops. 

It  is  interesting  to  note  that  in  both  of  these  cases  there  were  quite 
a  few  small  foci  of  old  focal  nephritis,  such  as  have  been  described  in 
diplostrei)tococcus  endocarditis  by  previous  observers.  This  was  also 
the  case  in  observation  3.  Evidently  for  many  years  the  kidneys  with- 
stood the  effect  of  continued  bacterial  embolism  fairly  well,  until  in  the 
end  they  more  or  less  suddenly  gave  way.     It  is  difficult  to  say  whether 


ACl'TK    C.I.OMKKri.O-MCI'HUI  I  l>  *) 

this  slimilil  lie  ascrihcd  t(i  an  iiurcaseil  vinilfiuc  on  tlic  ))art  nf  tin-  in- 
fectious organism  or  to  tlie  (K\  flopniint  of  a  liyperscnsitivencss  in  the 
organ.  It  appears  to  nie  tliat  mi  tlie  wliolc  the  last  view  is  the  more 
likely  one. 

The  third  case  is  remarkable  hecause,  in  spite  of  tiie  fact  that  an  old 
endocarditis  was  found  at  autojjsy,  there  were  no  clinical  symiitoms  to 
suggest  it.  The  fourth  case  is  one  of  cirrhosis,  with  the  usual  clinical 
manifestations.  In  both  of  these  last  cases  the  acute  nephritis  devcloi)ed 
in  the  last  three  weeks.  In  case  3  there  was  a  very  suggestive  history 
of  a  sudden  breakdown,  with  characteristic  disturbances  in  urination 
three  weeks  before  his  death.  The  patient  suddenly  had  to  urinate  very 
frequently,  and  developed  oedema.  In  case  4  there  is  no  such  detinile 
history  of  the  onset,  but  about  a  month  before  her  deatii  she  liccame 
much  worse,  this  being  some  time  after  tl-.e  development  of  se])tic  ulcers 
on  her  legs,  which  were  probably  the  cause  of  her  nephritis.  The  ne])hri- 
tis  in  these  cases  is  therefore  probably  about  three  to  four  weeks  old. 
Clinically  it  showed  by  the  develojiment  of  oedema.  .Some  jjuffiness  of 
the  face  is  recorded  in  case  4.  The  urine  in  both  cases  containeil  much 
albumin,  many  hyaline  and  gr.iiuilar  casts,  and  some  leucocytes. 

The  kidneys  were  greatly  swollen.  They  were  hyiwraemic  and 
oedematous.  The  cortex  was  wide,  more  or  less  yellowish,  and  o]ia(|ue. 
It  contained  petechial  haemorrhages.  Histologically  there  was  somewhat 
more  evidence  of  extracapillary  proliferation  in  the  glomeruli:  otherwise 
the  lesions  were  similar  to  those  observed  in  the  earlier  cases.  Many 
tubules  were  filled  with  blood  and  with  neutrophilic  leucocytes.  The 
epithelium  was  swollen,  somewhat  granular,  and  in  one  case  fatty  de- 
generation had  occurred.  The  interstitial  tissue  in  both  cases  was  heavily 
infiltrated  with  neutrophilic  leucocytes  and  with  lym|)hocytes.  In  case  4 
there  was  already  evidence  of  a  beginning  jiroliferation  of  the  connective 
tissue  cells.  That  this  proliferation  was  of  inflammatory  origin  is  so 
evident  that  it  docs  not  admit  of  any  discussion.  In  some  of  the  glom- 
eruli also  a  beginning  organization  of  the  necrotic  material  had  set  in. 
In  the  one  case  in  which  the  tissues  examined  were  sufficiently  well  jire- 
served  for  bacteriological  examination  no  bacteria  were  found,  in  sjiite 
of  long  continued  search  with  the  mechanical  stage  through  several 
sections. 

In  all  four  cases  of  acute  glomerulo-ncphritis  the  etiology  was 
clearly  evident.  There  was  streptococcic  infection  with  bacteriaemia  in 
all,  and  in  three  the  nephritis  occurred  in  the  final  stages  of  an  old  dijilo- 
streptococcic  endocarditis.  The  death  of  these  four  patients  is  largely 
attributable  to  their  ])re-existing  disease,  and  it  was  for  this  reason  that 


10  Till-:    rATIlnl.OG'i'    OF    NICPIIRITIS 

there  was  an  oppDrlunity  of  stiulsinn'  llie  alterations  in  tlie  kidneys  at 
this  early  stage. 

In  the  very  beginning  the  lesions  are  practically  confined  to  the 
glomeruli,  the  initial  change  being  a  hyaline  thrombosis  of  some  of 
the  vascular  loops,  followed  by  necrosis  and  an  infiltration  of  tlie  entire 
glomerulus  with  neutrophilic  leucocytes.  Naturally  in  ordinary  sections 
not  all  affected  glomeruli  show  the  necrotic  loops,  but  my  impression  is 
that  in  a  series  one  can  always  find  them  in  each  affected  glomerulus. 
The  diseased  glomeruli  bleed  and  permit  of  the  passage  of  albumin  and 
leucocytes — w-hich  explains  the  material  found  in  the  ca])sular  spaces,  in 
the  tubules,  and  in  the  urine.  Sometimes  the  exudate  has  a  tendency  to 
spontaneous  coagulation  in  the  capsular  spaces  and  in  the  tubules. 

\'ery  soon  these  glomerular  lesions  are  followed  by  a  general  hyper- 
acmia  and  oedema  which  causes  considerable  enlargement  of  the  organ. 
Tile  oedema  often  is  very  pronounced.  The  hyperaemic  blood-vessels 
show  a  marked  local  leucocytosis,  numerous  venules  in  the  region  of 
the  vasa  recta  being  especially  engorged  and  full  of  various  types  of 
leucocytes.  The  congestion  is  soon  followed  by  a  general  extravasation 
of  leucocytes  into  the  tissues,  the  intensity  of  the  reaction  naturally 
depending  on  the  severity  of  the  process.  Among  the  leucocytes  that 
find  their  way  into  the  tissues  there  are  many  neutrophilic  cells,  together 
with  lymphocytes  and  plasma  cells,  as  can  easily  be  seen  in  sections 
stained  with  Giemsa's  stain  according  to  Schridde's  method.  The  amount 
of  epithelial  degeneration  also  naturally  varies  with  the  intensity  of  the 
process.  In  some  of  our  cases  it  is  noted  as  slight,  in  others  it  is  ciuite 
considerable.  There  is  no  question  that  the  disturbance  in  circulation 
and  the  oedema  as  such  must  be  important  factors  in  the  development 
of  these  degenerative  lesions ;  still  one  can  hardly  escape  recognizing 
also  the  importance  of  a  toxic  factor.  The  possible  epithelial  lesions  at 
this  time  consist  in  swelling,  with  slight  granular  degeneration,  fatty 
degeneration,  and  scattered  necroses. 

As  a  result  of  the  inflammatory  oedema  the  connective  tissue  cells 
of  the  interstitial  tissue  become  swollen.  After  a  few  weeks,  evidences 
of  proliferation  may  be  observed  on  their  part.  As  has  been  stated 
above,  of  the  inflammatory  nature  of  this  proliferation  there  can  be  no 
doubt. 

In  the  glomeruli  also  proliferative  changes  occur  quite  early  in  the 
process.  The  capsular  epithelium  swells,  is  partly  detached,  and  pro- 
liferates somewhat.  My  impression,  however,  is  that  the  majority  of  the 
new  cells  in  the  glomeruli  which  become  so  plentiful  in  the  later  stages 
are  derived   from  the  connective  tissue,  both  of  the  capsule  and  of  the 


ACL'Ti-;  (;i.<i.mi-;kii.(i-ni:i'Mki  I  IS  11 

stalk  of  tlie  j^lnnuriihis.  I'liu  prolitcralix  i-  process  in  ihc  L;loimTiili  also 
is  partly  <listiiu'tl\  inllamniatory  ;  in  pari,  iiowcvcr.  it  is  in  the  nature  of 
an  organization  of  the  necrotic  material  ])roduced,  or  (jf  ileixisits  of  filirin 
which  are  a|)t  to  occur  in  the  capsular  s])ace. 

Of  the  origin  of  the  apparently  initial  hyaline  tlironiliosis  and  necro- 
sis of  some  of  the  vascular  Ioojjs  of  the  glomeruli,  1  have  sjjoken  at 
length  in  m\  previous  article.  Suflfice  it  to  state  here  that  it  ap|)ears 
proliahle  to  me  tiiat  it  may  be  due  to  ra])id  lytic  destruction  c)f  bacterial 
emboli,  with  liberation  of  haemolytic  and  necrotizing  endo-toxins. 

The  slight  lesions  in  the  larger  arteries  in  the  kidnevs  and  else- 
where wliicii  arc  noted  in  the  i>n)tocols.  are  naturally  purely  incidental. 

I  ni.iy  state  at  this  ])oint  that  for  brevity's  sake  in  the  protocols  I 
ha\e  \i^fd  tlie  terms  "arteriosclerosis"  and  "endarteritis"  in  the  sense  of 
Jores.  employing  "arteriosclerosis"  when  there  was  a  notable  hy|)erplasia 
of  the  elastic  elements  of  the  intima.  The  distinction,  however,  is  meant 
to  be  a  ])urely  morphological  one.  not  implying  the  deejier  --ignificance 
attributed  to  it  by  Jores. 


12  Till-;    I'ATUOl.OGV   01'    NICIMIRITIS 


II.  SuiiACUTF,  (Ii.omkkulo-N'ki'iikitis  (Cases  5-12). 

Naturally,  there  exists  no  sharp  line  of  division  between  the  acute, 
subacute,  and  chronic  cases.  Cases  5  and  (\  for  instance,  might  just  as 
well  have  been  classified  with  the  acute,  and  cases  11  and  12  with  the 
chronic  types. 

The  beginning"  and  the  course  of  the  disease  were  very  cliaracter- 
istic  in  case  5.  The  patient's  trouble  commenced  with  an  attack  of 
tonsillitis  about  nine  months  before  she  died.  Soon  symptoms  of  acute 
polyarticular  rheumatism  made  their  appearance,  and  continued  inter- 
mittently for  about  six  months.  The  severe  endocarditis,  which  evidently 
developed  simultaneously,  was  overlooked  until  the  patient  entered  the 
hospital  in  the  last  stages  of  the  disease.  At  that  time  she  already 
showed  evidence  of  severe  renal  involvement.  It  is  not  apparent  from 
the  history  when  her  renal  disease  started.  How  far  her  oedema  was  as- 
sociated with  her  nephritis  is  difficult  to  tell :  but  there  are  certain  symp- 
toms recorded  in  the  history,  like  frequent  vomiting,  restlessness,  drow- 
siness, muscular  twitching,  which  arouse  the  suspicion  of  a  uraemic 
condition.  Her  blood  pressure,  in  spite  of  the  severity  of  her  renal  com- 
plication, was  not  afifected,  possibly  on  account  of  the  severe  sejJtic  in- 
volvement of  the  heart  muscle.  Diplo-streptococci  were  recovered  during 
life  from  blood  and  urine,  and  after  death  from  the  infected  heart 
valves. 

The  following  case  (6)  is  an  interesting  one  on  account  of  the  fact 
that  the  infection  which  caused  the  nephritis  was  apparently  caused  by 
colon  bacilli,  no  evidence  of  streptococcus  infection  being  discovered 
either  during  life  or  at  necropsy.  On  account  of  the  fact  that  the  child 
had  congenital  syphilis,  it  might  be  suggested  that  the  lesions  in  the 
kidneys  also  were  of  syphilitic  origin  ;  but  so  long  as  we  know  so  little 
of  the  histology  of  acute  and  subacute  syphilitic  nephritis,  I  believe  we 
would  hardly  be  warranted  in  making  this  assumption.  In  other  words, 
I  do  not  believe  that  the  proof  has  yet  been  furnished  that  spirochetes 
can  produce  lesions  in  the  kidneys  similar  to  those  observed  in  ordinary 
bacterial  infections. 

The  next  case  (7)  is  a  good  example  of  how  inattentive  some  patients 
are  to  the  state  of  their  health.  The  first  symptom  that  attracted  this 
patient's  attention  was  a  hemiplegia  and  aphasia  as  a  result  of  embolism 
from  a  severe  diplostreptococcus  endocarditis.  The  urinary  findings 
were  unusually  slight  for  the  severe  lesions  in  his  kidneys.  Except  for 
the  general  oedema,  which  of  course  may  be  attributed  to  his  cardiac 
disease,  there  were  no  other  general  symptoms  of  nephritis. 


SUUAITTK    f.l.OMKKll.O-NKl'MKITIS  1.^ 

Ill  paiicin  S.  wliu  liad  an  ohj  streptococcus  infection  of  a  compound 
iraclure  of  the  lc,n.  the  urinarv  tindings  made  the  diagnosis  of  nephritis 
eviilent.  I  "here  was  some  oedema,  but  it  was  not  very  marked  at  any 
time.  C)ther  "nephritic"  symptoms  were  cnm])lctely  absent,  in  s])ite  of 
\  ery  severe  lesions  in  the  kidneys. 

In  case  9  the  renal  disease  was  only  a  minor  incident  in  tlie  typical 
clinical  develo])ment  of  a  severe  septic  endocarditis,  iirobal)ly  arisinjj 
ei,c:ht  months  before  death  from  infected  wounds  on  the  lins^ers.  Still, 
the  urinary  tindintis  were  unmistakable  and  the  phenolsulphone-phthalein 
excrelion  was  distinctly  slowed.  Three  months  before  his  death  the 
patient  liad  noticed  some  oedema  at  ihe  ankles,  increased  thirst,  and  in- 
creased urination.  The  oedema  at  no  time  was  a  prominent  symptom. 
and  was  absent  at  death. 

Case  10  is  notewnrthy  in  several  particulars.  The  patient,  a  nouul; 
woman,  liad  h,id  an  unusually  severe  long-continued  infection,  develop- 
ing from  a  decayed  tooth  about  one  \ear  before  her  death.  .\n  abscess 
e\entiially  formed  at  the  lower  jaw  which  had  to  be  drained  from  the 
outside.  I-'ollowing  the  operation  the  abscess  healed,  and  at  necropsy 
a  small  scar  only  could  be  found  at  the  place  where  it  had  been.  Several 
decayed  teeth,  however,  remained  in  her  mouth.  .After  the  healing  of 
the  abscess  she  was  apparentlx'  well  until  four  weeks  before  her  death, 
when  she  developed  a  painless  oedema  of  the  legs.  Ten  days  later  the 
right  leg.  which  was  still  oedematous,  became  infected  with  streptococci, 
from  which  infection  she  died  within  a  short  time. 

The  histological  picture  of  the  lesions  in  tlu-  kidneys  in  this  case 
differs  from  that  of  other  cases  of  this  series  by  the  lack  of  evidence  of 
actively  progressive  inflammation.  The  alterations  were  very  extensive, 
but  ai)parently  not  very  severe,  and  almost  (|uiescent.  .Almost  all  of  the 
glomeruli  were  diseased.  They  showed  development  of  fibrous  tissue 
Iietween  the  vascular  loops,  making  the  tufts  thick  and  heavy.  There 
was  also  some  little  proliferation  in  some  of  the  capsules  and  in  the 
capsular  spaces.  Although  so  many  glomeruli  were  diseased,  one  did  not 
receive  the  impression  that  theymajority  were  functionally  badly  dam- 
aged. The  newly  formed  fibrous  tissue  was  found  on  the  inside  of  the 
tufts,  and  did  not  therefore  apparently  interfere  much  with  the  secretion 
of  the  urine-water:  and  the  vascular  looi>s  themselves,  although  some  of 
them  showed  a  slightly  thickened  hyaline  wall,  ai)peared  otherwise  nor- 
mal. Many  tubules  were  filled  with  hyaline  casts,  and  some  of  them 
with  neutrophilic  leucocytes.  The  epithelial  degeneration  which  was 
jireseiit  in  the  tubules  was  probably  recent,  and  to  be  attributed,  at  least 
in  jiart,  to  the  streptococcus  sepsis   from  which  the  patient  died.     The 


14  Tin-;    I'A'IIKll.UC'i-    (IF    MJMIKITIS 

arteries  were  ])raclic:ill\  iKirmal.  except  the  main  stems  of  the  renal  ar- 
teries, which  were  moderately  sclerosed.  On  the  whole,  therefore,  the 
histological  picture  would  suggest  that  the  process  was  fairly  well  healed, 
at  any  rate  rather  (|uiescent.  Clinically,  however,  the  evidences  of 
renal  disease  were  well  marked.  Her  first  symptom,  the  oedema,  was 
evidently  a  "renal"  oedema,  because  there  were  no  signs,  either  clinical 
or  anatomical,  of  cardiac  decomjjensation.  There  was  also  distinct  hyper- 
tension, and  a  slight  but  unmistakable  hypertrophy  of  the  left  ventricle. 
The  urinary  findings  also  were  well  marked.  Although  the  urinary 
production  was  diminished,  the  specific  gravity  was  fixed  at  about  loio; 
there  was  much  albumin  in  the  urine,  and  many  formed  elements  in  the 
sediment.     Symptoms  of  uraemia,  however,  were  altogether  absent. 

In  the  following  case  (  1 1  )  we  have  subacute  nephritis  in  an  indi- 
vidual suffering  at  the  same  time  from  old  diplostreptococcic  endocardi- 
tis and  syphilitic  aortitis  with  aneurysm.  The  time  when  the  diplo- 
streptococcus  infection  took  place  cannot  any  more  be  established  exactly, 
but  the  patient  complained  of  heart  trouble  for  at  least  four  years  before 
his  death.  As  shown  by  a  history  of  extreme  polyuria  half  a  year  before 
his  end,  his  nephritis  must  have  dated  back  before  this  time.  The 
polyuria  in  this  case  was  a  striking  and  constant  symptom,  and  possibly 
accounts  for  the  comparative  absence  of  oedema.  His  symptoms  were 
largely  those  of  endocarditis,  complicated  naturally  by  the  co-existing 
aortic  aneurysm.  His  blood  pressure  was  high  and  rising.  His  heart 
was  twice  normal  size,  an  enlargement  partly  due  to  aortic  regurgitation. 
His  urine,  on  account  of  the  polyuria,  naturally  had  a  constant  low 
specific  gravity ;  it  contained  much  albumin  and  many  formed  elements. 
While  he  was  at  the  hospital  there  was  practically  no  excretion  of  phenol- 
sulphone-phthalein.  The  pericarditis  which  he  developed  eventually  was 
due  to  an  extension  of  the  dijilostreptococcic  infection  from  the  heart 
valves  to  the  pericardium. 

In  the  last  case  (  12)  the  nejihritis  is  evidently  much  older  than  in 
the  others  of  this  series.  This  patient  had  had  numerous  attacks  of 
tonsillitis  from  infancy.  Six  years  before  death  her  nephritis  had  been 
first  noticed.  For  the  last  five  years  she  had  had  definite  "uraemic" 
symptoms  (headache  and  vomiting),  and  occasionally  slight  oedema. 
The  most  interesting  feature  in  this  patient's  history  was  that  she  had 
associated  with  her  nephritis  what  appeared  to  be  typical  symptoms  of 
"Raynaud's  disease,"  attacks  of  syncope  and  cyanosis  in  fingers  and  toes. 
Eventually  she  developed  an  anaemic  (  ?)  contracture  of  her  left  arm  and  a 
dry  gangrene  of  her  left  foot.  This  symptom-complex  was  probably  due 
to  a  o-radual  closing  of, her  peripheral  arteries  by  lateral  thrombosis  and 
endarteritis.      I'n fortunately  we  were  not  permitted  to  verify  this   sup- 


SUUAl  ITI-:    (J.dMl-.Kll.lP-M-.l'IIKIllS  15 

position  at  aiitoi)s\  ;  l>ut  uc  lia\c  I'vidiiut-  that  Ikt  internal  arteries, 
more  especially  those  in  the  heart  and  kidneys,  were  fjraduaily  i>eing 
closed  hy  such  a  process.  In  hotii  of  these  ortjans.  as  a  conse<|nence, 
small  multiple  necroses  resulted,  which  in  the  heart  were  irrei^ularly 
scattereil,  and  in  the  kidney  were  situated  in  the  pyramids,  liacteria 
were  not  found  in  the  small  arteries  which  were  the  seat  of  the  throm- 
bosis. Towards  the  end  a  similar  thrombotic  obstruction  took  ))lace  in 
some  of  the  arteries  of  the  sigmoid  flexure,  with  much  bleeding  and  ex- 
tensive sloughing.  .Ml  these  processes  naturally  at  first  suggested  the 
occurrence  of  multiple  embolism:  but  no  source  of  embolism  was  dis- 
covered in  the  pulmonary  vein,  left  heart,  or  the  aorta:  besides,  tlie 
gradual  development  of  the  conditions  in  the  extremities  speaks  very 
much  against  embolism  as  the  causative  factor,  and  favors  the  idea  of 
their  origin  by  gradual  thrombosis. 

The  case,  1  believe,  is  of  unusual  imixirtance.  because  it  seems  to 
furnish  the  proof  that  tin-  Literal  thrombosis  followed  by  endarteritis, 
which  is  so  frequently  observid  in  llu-  kidneys  in  these  cases  of  glom- 
erulo-nephritis  (see  below),  may  involve  arteries  in  other  parts  of  the 
body,  and  may  in  this  way  give  rise  to  symptoms  resulting  from  a  more 
or  less  gradual  obstruction  of  them.  .\"o  doubt  sometimes  the  cerebral 
arteries  may  be  involved  in  the  same  way.  That  this  i)atient,  in  spite  of 
the  absence  of  an  infectious  endocarditis,  suffered  from  a  chronic  di])lo- 
streptococcus  bacteriaemia,  at  least  as  long  as  she  was  under  clinical 
observation,  seems  evident.  She  had  a  septic  temperature  all  the  time. 
Her  pulse  rate  varied  between  80  and  130,  and  the  blood  culture  was 
positive.  In  fact,  clinically  there  seemed  to  be  no  doubt  that  the  patient 
had  a  septic  endocarditis,  and  the  absence  of  this  condition  at  autopsy 
was  a  great  surprise.  In  fortunately,  a  thorough  search  for  another 
chronic  septic  focus  could  not  be  made.  It  is  possible  that  in  this  in- 
stance the  urinary  tract  itself  may  have  harbored  the  diplococci,  because 
there  was  evidence  at  necro])sy  of  a  slight  chronic  sujipurative  ])yelitis 
and  cystitis  with  positive  finding  of  diplostreptococci.  This,  however, 
may  have  been  merely  the  conse(|uence  of  the  constant  elimination  of 
diplostrejJtococci  by  way  of  the  kidneys. 

This  jjatient's  "nephritic"  complications  were  uiuuistakable.  .She 
had  headaches  and  vomiting:  she  had  albuminuric  retinitis:  she  had 
comparatively  little  oedema :  she  had  a  high  blood  (iressure  with  clinical 
signs  of  excessive  heart  action,  but  without  gross  hyijcrtrojihy :  she  died 
in  uraemic  coma.  The  urinary  findings  also  were  very  well  marked.  She 
had  some  symptoms  suggesting  jjolyuria.  a  fixed  low  si)ecific  gravity. 
The  urine  contained  much  albumin,  and  at  times  there  were  large  show- 
ers of  casts.     Red  blood  cells  were  also  commonlv  found. 


16  Till':  ^ATll()l,(l(;^   oi'  xkimikitis 

To  sum  u|>:  In  all  these  cases  of  siiliaciitc  nephritis,  except  in  case 
6,  there  can  hardly  be  any  question  of  the  etiology;  and  in  this  one  I  am 
inclined  to  believe  that  the  nephritis  was  due  to  a  colon  bacillus  septi- 
caemia arising  from  the  infected  urinary  tract.  In  the  cases  with  endo- 
carditis ( 5,  7,  <;.  Ill  chronic  diplostreptococcus  septicaemia  existed, 
without  doubt ;  in  case  8  a  chronic  streptococcus  septicaemia  from  the 
infected  bone  is  also  ver)-  likely;  and  in  case  12  the  clinical  symptoms 
and  the  positive  blood  culture  proved  the  existence  of  a  chronic  septi- 
caemia, at  least  as  long  as  the  patient  had  been  under  clinical  observation. 
The  source  of  the  continued  infection  in  this  case  was  possibly  in  the 
urinary  tract.  The  only  somewhat  questionable  case  is  case  10,  where  the 
original  septic  infection  was  present  in  the  region  of  the  jaw,  where, 
however,  after  long  treatment  the  lesion  eventually  healed.  \o  ])ersist- 
ing  septic  focus  was  definitely  made  out,  although  she  still  had  several 
decayed  teeth  ;  and  it  is  possible  that  the  histological  evidence  of  com- 
parative quiescence  of  the  process  in  the  kidneys  might  indicate  that 
whatever  infection  remained  was  not  very  active  or  extensive. 

The  clinical  symptoms  of  nephritis  were  quite  definite  in  all  cases. 
All  of  them  had  oedema  at  one  time  or  another,  the  amount  of  oedema 
and  its  distribution  varying  very  much  in  different  cases.  One  early  case 
(S)  had  somewhat  indefinite  symptoms  of  uraemia;  otherwise  the  others 
were  free  from  it,  except  the  most  chronic  case,  which  was  much  older 
than  the  rest,  in  which  there  were  observed  very  definite  uraemic  symp- 
toms and  a  well  marked  retinitis  albuminurica. 

Case  8,  of  about  six  months'  duration,  already  showed  a  beginning 
hypertrophy  of  the  left  ventricle ;  and  the  last  three  cases  had  a  definite 
rise  of  systolic  blood  pressure  to  between  170-200  mm.  mercury,  and  two 
of  them  a  noticeable  hypertrophy  of  the  left  ventricle.  In  the  case  (ill 
with  very  marked  hypertrophy  of  the  heart,  the  hypertrophy  w-as  probably 
largely  due  to  valvular  disease. 

The  urinary  findings  were  striking  in  all  cases.  The  urine  at  all 
times  contained  much  albumin.  Casts  (  hyaline,  granular  and  epithelial ) 
were  almost  just  as  constantly  present,  although  sometimes  they  were  not 
found  at  all  times,  but  in  showers.  Leucocytes  and  erythrocytes,  either 
free  or  as  blood  casts,  were  also  commonly  encountered.  Two  cases  (9 
and  II)  had  a  definite  polyuria,  which  was  extreme  in  case  ir.  In  the 
more  chronic  cases  (10,  11,  12)  the  specific  gravity  was  fixed  at  a  low 
point,  not  always  apparently  as  a  result  of  polyuria,  the  condition  being 
suggestive  of  a  true  hyposthenuria. 

In  case  9  the  phenolsulphone-phthalein  excretion  was  somewhat 
slowed,  in  case  11  entirely,  suppressed,  and  in  case  12  very  much  delayed. 


si'hai  r  ii-.  i;i.(iMKKii.i)-M;niKiris  17 

III  tlu-  ^ross,  tlu-  kidiR'vs  were  smootli,  conj^cstcil,  (n.'(leiiiat>piis  anil 
swollen,  or  already  contracted  to  about  normal  size.  Tiic  cortex  was 
either  dilTuseJy  opac|ue  or  contained  small  opaque  spots.  Petechial  cort- 
ical haemorrhai:jcs  were  often  seen.  They  were  most  numerous  in  case  5 
(see  fig.  7).  Histologically,  in  the  more  acute  cases  the  tissues  were  still 
much  infiltrated  with  neutrojihilic  leucocytes,  to  which  were  n<iw  added 
many  eosinojjhilic  and  basophilic  cells.  The  glomeruli  in  most  cases 
showed  a  very  general  intense  intra-  and  e.xtra-capillary  jiroliferation.  In 
the  more  chronic  cases  many  of  them  had  already  become  fibrous.  The 
tubules  were  full  of  blood.  neutro|)hilic  leucocytes,  and  casts.  The 
amount  of  degeneration  in  the  epithelium  of  the  tubules  varied,  being 
intense  in  some  cases  and  rather  light  in  luiicrs.  without  much  reference 
to  the  severity  of  the  lesions  elsewhere.  In  all  cases  the  interstitial 
tissue,  in  addition  to  being  infiltrated  with  lymphocytes  and  granular 
leucocytes,  showed  evidence  of  considerai)le  fairly  diffuse,  inflammatory 
proliferation,  which  in  the  later  stages  had  already  commenced  to  en- 
croach upon  the  tubides  in  some  places. 

The  arteries  in  the  kidneys  were  normal  in  cases  5,  6,  7,  and  9.  In 
case  8  the  slight  arterial  lesions  were  evidently  purely  incidental,  which 
is  probablj-  also  true  in  case  10;  hut  in  case  11  definite  lesions  were  found 
in  some  of  the  arterioles  and  larger  Itlood-vessels,  which  must  be  asso- 
ciated with  the  nephritis:  and  in  case  12  the  arterial  involvement  was 
unusually  well  marked.  The  lesions  in  these  last  cases  seem  to  extend 
back  from  the  affected  glomeruli  into  the  arterioles,  and  to  consist  in 
lateral  hyaline  thrombosis,  with  rapid  organization  leading  to  endarter- 
itis. In  the  cellular  newly-formed  connective  tissue  in  the  intima  there 
are  practically  no  elastic  fibers,  as  is  well  shown  in  fig.  18.  In  the  larger 
arteries,  on  the  other  hand,  there  is  no  evidence  of  such  a  process ;  but 
there  is  present  a  definite  hyperplastic  thickening  of  the  elastic  tissue  of 
the  intima. 

The  arteriosclerosis  found  in  other  parts  of  the  Ijody  in  cases  8,  11 
and  12  can  almost  certainly  be  looked  upon  as  being  unconnected  with 
the  renal  disease.  Cases  10,  11,  and  12  demonstrate  clearly  that  the 
blood  pressure  rises  and  remains  constantly  elevated  before  there  are 
anatomical  signs  of  general  arterial  disease.  The  rise  in  pressure  must 
be  due  to  some  functional  disturbance  in  arteries  and  heart,  which  throws 
out  of  action  the  regulatory  mechanism  which  normally  maintains  tlie 
blood  pressure  at  such  a  remarkably  constant  level. 

The  anaemia  which  was  present  in  all  cases  is  in  all  probability  to 
be  attributed  to  the  chronic  sepsis,  rather  than  to  the  disease  of  the 
kidneys. 


18  THE   PATHOLOGY   OF   NEPHRITIS 


III.  Late  Subacute  Glomerulo-Nephritis  ix  Children  (Cases  13-15) 

The  following  three  cases  are  of  special  interest  because  they  show 
the  effects  of  continued  nephritis  on  the  youthful  organism.  The  patients 
were  children  between  6  and  10  years  of  age.  The  possibility  of  arter- 
iosclerosis complicating  the  condition  can  be  positively  excluded  in  these 
cases,  and  as  a  matter  of  fact  no  general  disease  of  the  blood-vessels  was 
observed  in  any  of  them.  Whatever  cardio-vascular  disturbances  were 
observed  in  these  instances  must  therefore  be  in  some  way  associated 
with  the  disease  in  the  kidneys. 

The  first  of  these  cases  (13)  had  no  history  of  any  acute  infections 
except  the  milder  types  of  diseases  of  childhood.  The  possibility  of  her 
having  had  an  attack  of  tonsillitis,  rheumatism  or  scarlet  fever  was  pos- 
itively denied  on  repeated  questioning,  which  is  remarkable  and  shows 
that  the  diplostreptococci  sometimes  enter  without  provoking  severe 
symptoms,  because  at  necropsy  it  was  discovered  that  she  did  suffer  from 
an  old  diplostreptococcic  infection  of  the  aorta. 

Her  first  symptoms,  five  months  before  death,  were  of  a  uraemic 
nature,  of  that  type  which  gives  rise  to  headaches,  vomiting  and  convul- 
sions. The  convulsions  in  this  patient  were  not  very  severe.  They  were 
frequently  followed  by  periods  of  amaurosis,  probably  due  to  spasm  in 
the  retinal  artery. 

In  addition  to  this  functional  and  more  or  less  transitory  condition, 
organic  lesions  later  developed  in  the  fundus  of  her  eyes ;  optic  neuritis 
and  retinitis,  and  a  detachment  of  the  retina  in  the  left  eye.  After  a 
while  increased  thirst  and  polyuria  was  noticed.  She  had  remarkably 
little  oedema  of  the  skin  (slight  puffiness  of  the  face  at  one  time).  Her 
polyuria  with  low  specific  gravity  continued  to  the  end.  Otherwise  the 
urinary  changes  were  not  very  pronounced ;  the  urine  containing  little 
albumin,  few  casts,  and  some  leucocytes.  Her  systolic  blood  pressure 
was  about  140.  The  clinical  signs  were  pre-eminently  those  of  a  severe 
sepsis  (continued  fever  and  leucocytosis),  and  the  general  findings  and 
also  the  local  ones  in  the  region  of  the  heart  again  suggested  strongly 
endocarditis,  as  in  case  12.  Contrary  to  all  expectations,  no  endocardial 
lesion  was  discovered  at  autopsy,  but  an  infectious  aneurysm  in  the  upper 
part  of  the  abdominal  aorta  in  which  there  were  numerous  diplostrepto- 
cocci, and  a  severe  glomerulo-nephritis  with  considerable  shrinkage  of 
one  kidney."    The  cardiac  hypertrophy  which  had  been  noticed  clinically 


2  The  only  clinical  symptom  of  the  aneurysm  had  lieen  obscure  pa 
upper  abdominal  region. 


I.ATB-:    SUBACUTE   cr.OMERl'I.O-N'KPIl  RITIS    IN    CIIIIIIKKX  1'' 

and  had  been  ascribed  to  tlie  suspected  endocarditis,  turned  out  to  be  due 
entirely  to  the  "nepliritic"  hypertension.  In  tliis  case  the  arteries  were 
normal,  grossly  and  microscopically,  in  kidneys  and  elsewhere,  with  the 
one  exception  of  the  arterioles  in  the  spleen. 

Patient  14,  a  girl  of  10  years,  had  had  fre(|uent  attacks  of  tonsillitis. 
She  had  a  septic  temperature  on  a  subnormal  base  at  about  96°  I',  also 
continually  some  leucocytosis ;  but  the  old  septic  focus,  which  evidently 
existed  somewhere  in  her  body,  was  not  discovered  at  autopsy.  The 
first  symptoms,  which  appeared  two  years  before  death,  were  more  of  a 
cardiac  nature  (precordial  pain  and  dyspnoea)  ;  and  in  her  last  attack 
the  symptoms  of  broken  compensation  were  the  prevailing  ones.  To- 
wards the  end  she  was  very  restless  and  in  a  semi-comatose  condition, 
probably  as  a  result  of  true  uraemia.  Her  blood  pressure  was  quite  high 
(160)  for  a  child  of  her  ag3.  and  the  necro])sy  revealed  marked  hyper- 
trophy of  the  heart,  which  was  especially  well  developed  on  the  left  side. 
The  urine  contained  much  allmniin  and  lalher  few  casts,  also  a  few 
erythrocytes  occasionally. 

The  last  one  of  these  cases  (151  showed  a  definite  localization  of  the 
septic  focus  in  the  urinary  tract.  The  involvement  of  the  kidneys  was 
not  due  to  ascending  infection,  but  it  was  in  the  nature  of  a  true  haema- 
togenous  glon-.erulo-nephritis  (see  fig.  27).  Two  years  before  this  little 
boy"s  death  a  large  stone  was  removed  from  his  bladder.  .\t  that  time 
already  infection  of  his  bladder  was  evident,  and  this  infection  with 
streptococci  continued  to  his  end.  Cardiac  and  renal  symptoms  (poly- 
uria) developed  five  months  after  the  oi)eratii)n,  and  he  died  in  uraemic 
coma.  In  this  case  also  the  cardiac  hypertro|)hy  was  well  marked,  more 
especially  on  the  left  side. 

In  these  three  cases  of  late  subacute  ne])hritis  in  ciiildren.  then,  the 
cardio-vascular  disturbances  were  very  i)rominent  clinically,  and  the 
cardiac  hypertrophy  well  developed  anatomically.  Cases  like  these  furn- 
ish the  best  proof  that  the  hypertension  is  closely  associated  with  the  dis- 
ease in  the  kidneys,  but  does  not  necessarily  depend  upon  the  extent  of 
destruction  of  renal  tissue.  In  case  15  the  amount  of  functionating  renal 
tissue  left  is  very  small ;  still  the  cardiac  hypertro[)hy  is  quite  insignificant 
in  comparison  with  that  observed  in  case  13,  in  which  the  damage  to  the 
kidneys  is  evidently  much  less  extensive.  In  the  growing  body  of  a  child 
the  response  of  the  heart  muscle  by  hypertrophy  to  the  increased  work 
seems  to  be  unusually  rapid  and  extreme.  That  arterial  spasm  plays  some 
role  in  the  production  of  the  hypertension  is  strongly  suggested  in  case 
13,  in  which  the  tendency  to  spasmodic  contraction  was  so  well  marked 
in  the  retinal  arterv  and  was  directly  observed  by  means  of  the  ophthal- 


20  TllK    rATllOI.OCV   OK    NEPHRITIS 

moscope.  1 1.  from  the  behavior  of  this  one  artery,  one  could  arrive  at  a 
definite  conclusion  as  to  the  state  of  the  rest  of  the  small  arteries,  the 
evidence  would,  of  course,  be  more  convincing;  but  unfortunately  such 
is  not  the  case. 

Oedema  was  observed  in  two  of  these  three  cases,  but  it  was  not  a 
prominent  feature  in  any  of  them.  Clinically  a  certain  puffiness  of  the 
face  was  practically  all  that  was  noticed.  In  the  last  case,  at  autopsy  all 
tissues  were  found  to  be  unusually  dry.  In  this  connection  it  is  interest- 
ing that  the  existence  of  a  polyuria  is  especially  emphasized  in  the  records 
of  cases  13  and  15.  In  case  14  it  had  been  unfortunately  impossible  to 
determine  the  amount  of  urine.  In  cases  13  and  14,  however,  ascites  and 
hydrothorax  developed  in  the  end. 

In  case  13  the  urinary  findings,  apart  from  the  polxuria,  were  un- 
usually slight.  Repeated  examinations  failed  to  reveal  anything  more 
than  a  small  amount  of  albumin  and  occasionally  a  few  hyaline  casts. 
The  albumin  was  much  more  plentiful  in  case  14,  but  here  again  the 
number  of  casts  was  limited.  In  case  15  the  condition  of  the  urine  is 
unknown. 

"L'raemic"  symptoms  were  present  in  all  three  cases.  The  symptoms 
of  the  first  patient  started  with  headache  and  vomiting,  and  there  were 
imperfectly  developed  convulsive  attacks.  Whether  she  eventually  de- 
veloped true  uraemia  and  coma  is  unfortunately  unknown.  That  this 
condition  was  present  in  case  14  is  very  probable  from  the  history,  and 
certain  in  case  15. 

Whether  the  changes  in  the  backgrounds  of  the  eye  which  were  ob- 
served in  case  13  can  be  included  in  the  usual  picture  of  retinitis  albumin- 
urica  is  doubtful. 

The  anaemia  which  usually  accompanies  chronic  sepsis  and  nephritis 
was  present  in  all  cases,  but  to  a  moderate  degree  only. 

The  kidneys,  except  for  the  one  large  kidney  in  case  13,  were  ir- 
regularly contracted.  In  cases  13  and  15  they  showed  large,  deep,  irreg- 
ular scars  ;  in  case  14  they  were  more  finely  granular.  The  unusually 
small  size  of  the  one  kidney  in  case  14  is  probably  partly  due  to  disturb- 
ances arising  from  the  stenosis  of  its  ureter  by  a  congenital  fold. 

The  microscopical  appearance  of  the  lesions  was  very  much  that 
which  has  been  described  in  the  later  cases  of  subacute  nephritis  in  adults, 
only  that  in  cases  14  and  15  in  places  the  development  of  the  fibrous 
tissue  was  more  massive  and  the  atrophy  of  the  tubules  in  these  areas 
further  advanced,  as  is  well  shown  in  figures  25  and  28.  The  inflam- 
matory character  of  the  connective  tissue  proliferation  was  again  very 
evident  in  all  cases.  Many  glomeruli  were  already  entirely  fibrous,  more 
especially  in  the  older  lesions. 


I. ATI-:  sriiAi  r  I  !■:  <.i.(imi.i(i  i  o-m  riii;:  ris   in   i  ii  ii  |)Ui:n  Jl 

It  was  case  15  wliidi  first  (Jcnioiistratfil  to  im-  the  lallacv  of  tho 
belief  tliat  from  tlie  a|>i)earance  of  tlie  .y;lomeriilar  remnant  one  c<inl<l 
determine  wliether  the  j^lomernhis  was  thrown  ont  of  function  l)y  arter- 
iosclerosis or  whether  it  was  destroyed  by  u;lomeriilo-nei)hritis.  It  is  true 
that  in  the  latter  case  the  fibrous  remnant  is  usually  badly  defined  and 
has  lost  all  semblance  to  a  glomerulus,  whereas  in  arteriosclerosis  the 
vascular  tufts  merely  collapse  and  are  surrounded  by  a  more  or  less  cres- 
cent-shaped thickened  hyaline  capsule.  If  in  s^lomerulo-nephritis  the 
lesions  are  mostly  capsular,  however,  a  \ery  similar  condition  to  that 
which  occurs  in  arteriosclerosis  may  be  observed  in  the  end.  This  may 
be  very  puzzling,  especially  when  it  is  associated  with  much  endarteritis, 
as  in  case  15.  It  is  for  this  reason,  I  believe,  that  many  cases  have  been 
classified  as  arteriosclerotic  ne]>liritis  which  really  belong;  to  "glomerulo- 
nephritis. 

The  local  condition  of  the  arteries  again  xaried  reiiiarkablv  in  this 
short  series.  In  case  1.^  tliey  were  entirely  normal.  In  case  14  the  small 
arteries  showed  a  well  marked  "endarteritis,"  and  in  some  of  the  larger 
ones  the  internal  elastic  membrane  was  split  up  into  several  thick  super- 
imposed layers.  gi\ing  the  typical  picture  of  a  hyperplastic  develojiment 
characteristic  of  true  arteriosclerosis  according  to  Jores.  In  case  15  the 
lesions  in  both  small  and  larger  arteries  were  in  the  nature  of  a  very 
jiroiiouuced  "endarteritis." 


THE  PATIIor.o(',^■  or  NF.niRiTis 


r\'.  Chronic  Gi.o.mkrulo-Nkphritis  (Cases  16-32). 

in  order  to  avoid  tedious  repetition  the  cases  of  tliis  last  scries  will 
We  taken  up  in  a  more  summary  fashion. 

Ever  since  the  disease  has  been  recognized  the  etiology  of  these 
chronic  cases  has  been  a  most  vexing  problem.  Whereas  in  the  acute 
and  even  the  subacute  cases  the  history  of  some  septic  infection  can 
usually  be  obtained  and  a  persisting  septic  focus  can  often  be  demon- 
strated fairly  easily,  in  the  chronic  cases  the  history  of  the  original  in- 
fection dates  back  so  far  that  it  often  is  entirely  forgotten  by  the  patient, 
especially  by  patients  who  are  more  or  less  indifferent  in  regard  to  the 
state  of  their  health ;  and  the  persisting  focus  apparently  may  be  so 
insignificant  that  an  unusually  careful  clinical  examination  and  even  an 
unusually  carefully  performed  necrojisy  may  fail  to  reveal  it.  In  these 
cases  the  original  infection  is  probably  often  due  to  organisms  of  a  low 
degree  of  virulence  which  provoke  very  slight  symptoms,  and  the  bacteri- 
aemia  also  is  comparatively  slight  and  intermittent,  as  one  would  expect 
from  a  comparatively  insignificant  and  hidden  focus. 

In  searching  for  the  time  and  character  of  the  original  infection  the 
question,  how  far  one  is  able  to  communicate  with  the  patient  and  his 
family,  is  of  great  importance;  so  that  in  patients  able  to  speak  foreign 
languages  only,  especially  such  languages  as  Chinese  and  Japanese,  it  is 
often  a  i)racticaliy  hopeless  task.  Many  of  these  patients  arrive  at  the 
hospital  in  a  comatose  condition,  and,  unless  close  relatives  or  friends  are 
accessible,  very  little  or  nothing  can  be  made  out  about  their  ante- 
cedents. 

Among  our  sixteen  cases  there  were  seven  (cases  16,  18,  20,  25,  27, 
29,  32)  in  which  for  one  reason  or  another  the  history  is  imperfect.  Of 
the  other  nine  patients  one  (17)  had  scarlet  fever  as  a  child  and  rheu- 
matism at  twenty  years  of  age.  another  (19)  claimed  to  have  been 
healthy  all  his  life.  He  even  denied  having  had  any  diseases  in  child- 
hood, which  makes  his  statements  somewhat  improbable.  Patient  21 
had  had  a  severe  infection,  "a  touch  of  typhoid,"  as  she  said,  at  the  age 
of  22,  and  her  symptoms  dated  from  the  time  she  was  23.  Patient  22  had 
had  a  long  continued  suppuration  of  the  neck  due  to  chronic  tuberculosis, 
necessitating  twelve  operations.  In  such  a  case  the  existence  and  persist- 
ence of  mixed  infection  with  septic  organisms  is,  of  course,  not  at  all 
unlikely.  In  the  history  of  patient  23  we  read  of  repeated  attacks  of 
tonsillitis  and  several  attacks  of  polyarticular  rheumatism.  Patient  24 
also  has  a  history  of  rheurnatism.     In  case  26  we  encounter  once  more  a 


LllRoNK    CI.O.MMUfl.o-NI'.niKms  2^ 

general  denial  oi"  all  diseases  except  measles  in  infancy.  In  case  JS  also 
there  is  no  statement  in  regard  to  the  original  infection.  I'aiieTit  ,^o  had 
had  trec|uent  attacks  of  sore  throat,  and  patient  ,^i  had  had  what  she 
called  "l,a  Grippe"  as  a  girl  and  an  attack  of  acnte  api>eiidicilis  nine 
years  before  her  death.  .\  direct  relation  of  the  original  infection  to  the 
following  nephritis  is  traceable  only  in  one  case  (21  )  ;  still  the  investi- 
gation shows  that  in  fully  six  of  the  nine  cases  the  existence  of  some  in- 
fection ]5rece<ling  the  nephritis  and  iikcl\'  to  provoke  nephritis,  coidd  be 
established. 

The  mere  ])resence  of  such  a  history  docs  not  of  course  |)rove  that 
the  nephritis  must  have  been  due  to  such  infection.  However,  in  this 
connection  we  have  to  consider  that  in  all  acute  and  subacute  cases  the 
relation  of  such  infections  to  the  nephritis  is  very  evident:  and  there  is 
no  reason  to  assume  that  the  clironic  cases  of  evidently  the  same  disease 
should  be  due  to  a  different  cause.  Considering  the  difficulties,  I  believe 
that  the  finding  of  a  history  of  a  suspicious  infection  in  six  out  of  nine 
complete  histories  is  (juite  suggestive — all  the  more  so,  as  in  one  of  these 
negative  cases  (28)  in  spite  of  the  denial  of  all  infection  and  in  the  ab- 
sence of  any  symptoms  observed  by  the  |)atient.  a  chronic  infectious  en- 
docarditis was  found  at  autopsy. 

Definitely  persisting  sejJtic  foci  were  found  in  the  sixteen  cases  as 
follows:  old  atheromatous  ulcers  infected  with  diplococci  in  case  16; 
old  ]>us  |)ockets  in  the  tonsils  with  considerable  scarring  in  case  20:  an 
old  healed  scar  at  the  base  of  the  aorta  and  an  old  septic  infarct  of  the 
spleen  full  of  influenza  bacilli  in  the  patient  (21  I  who  had  had  a  "touch 
of  typhoid"  thirteen  years  before  her  death  :  an  old  ulcerative  endo- 
carditis in  the  i)atient  (231  w'ho  had  a  history  of  tonsillitis  and  rheu- 
matism: an  old  ulcerative  endocarditis  in  case  28;  an  old  ulcerative 
tonsillitis  and  an  ajJiJarently  old  mild  suppurative  pyelitis  in  the  patient 
(31  I  who  had  had  the  attack  of  "La  Grippe,"  The  long  continuance  of 
the  rheumatic  infection  in  case  17  is  shown  by  the  fact  that  many  years 
after  his  original  trouble  he  developed  a  pleurisy,  evidently  on  a  rheimiatic 
basis,  because  there  was  no  evidence  of  tuberculosis  found  at  autojisy.  It 
is  also  to  be  noted  that  during  the  last  years  of  his  life  he  complaineil  for 
several  years  of  chills  in  the  evening  and  night  sweats.  In  case  32  there 
is  a  history  of  "malaria."  so  frequently  wrongly  diagnose<l  in  chronic 
sepsis:  and  in  case  30.  with  a  history  of  tonsillitis,  there  is  a  subse(|tient 
history  of  repeated  attacks  of  arthritis,  which  may.  however,  have  lieen 
gouty  in  character. 

.Mtogether  of  the  sixteen  cases  there  are  six  only  which  are  entirely 
negative  so  far  as  history  and  autopsy  findings  are  concerned  ;    and  of 


24  Till-;    I'ATIIOI.OCV    OK    NKl'HKITIS 

these,  four  have  imperfect  histories.  One  of  these  (  Hj)  had  a  chronic 
suppiirative  catarrh  of  the  rectum  due  to  diplostreptococcus  infection, 
and  a  diplostreptococcus  sepsis  at  autopsy.  There  was  no  way  of  de- 
termining the  age  of  this  infection,  because  the  infection  of  the  rectum 
had  not  been  noticed  by  the  patient,  but  was  accidentally  discovered  when 
a  routine  examinati(«i  of  the  rectum  was  made  after  he  had  entered  the 
hospital. 

No  really  careful  examination  of  the  nose,  the  accessory  sinuses,  the 
roots  of  the  teeth,  and  other  well  known  foci  of  chronic  septic  infection, 
was  made  in  these  cases  either  clinically  or  anatomically  :  and  I  believe 
the  result  should  encourage  us  to  search  more  carefully  for  such  condi- 
tions. Even  under  the  most  favorable  circumstances  we  can  hardly  hope, 
in  a  disease  which  often  lasts  twenty  years  and  more,  to  definitely  estab- 
lish its  relation  to  chronic  sepsis  in  more  than  a  majority  of  cases.  My 
impression  is,  that  the  original  infection  usually  takes  place  at  a  compara- 
tively early  age  (fifteen  to  twenty  years  and  longer  before  death  ),  and,  as 
is  clearly  shown  in  several  of  the  histories,  is  unfortunately  not  imme- 
diately followed  by  clear  symptoms  of  nephritis,  the  earliest  symptoms 
(possibly  indicating  renal  disease  and  consisting  of  headache  and  vomit- 
ing) having  been  observed  about  one  year  after  the  infection  in  case  21. 
Otherwise  the  damage  to  the  kidneys  is  not  noticed  at  the  time,  nor  the 
persistence  of  the  infection  in  some  more  or  less  hidden  focus.  Whether 
a  careful  clinical  examination  at  the  time,  with  urinanalysis,  etc.,  would 
reveal  the  seriousness  of  the  condition  remains  to  be  seen,  but  does  not 
seem  at  all  unlikely. 

In  such  an  early  discovery  of  the  real  seriousness  of  the  situation 
would  consist  the  only  hope  of  the  patient  for  a  permanent  cure,  by  the 
possible  eradication  of  the  septic  focus,  a  general  treatment  directed 
towards  increased  resistance  to  infection,  and  a  careful  symptomatic 
treatment  of  the  disease  of  the  kidneys.  My  belief  is,  that  the  acute 
nephritis  in  scarlet  fever  is  so  rarely  followed  by  chronic  nephritis,  be- 
cause in  the  first  place  the  septic  infection  in  scarlet  fever  is  self-limited, 
and  if  the  patients  recover,  heals  completely;  and  secondly,  because  the 
patients  usually  are  in  bed  under  professional  care  and  the  nephritis  often 
is  severe  enough  to  be  noticed  easily,  both  of  these  latter  circumstances 
assuring  proper  treatment.  In  the  more  obscure  septic  infections  neither 
the  original  disease  nor  the  nephritis  which  is  associated  with  it  may 
attract  sufiicient  attention  on  the  part  of  the  patient,  or  of  the  physician 
if  the  case  happens  to  be  brought  to  the  attention  of  a  professional  man. 

The  time  at  which  the  first  definite  "renal"  symptoms  make  their 
appearance  varies  very  much.    In  case  21  they  seem  to  have  followed  the 


ClIKONIC    C.l.dMllKli.o-Mll'llKI'llS  J> 

original  inui.li(in  within  tin-  year,  hut  iiMially  ten  years  or  nmrc  sccni  to 
ilai)se  hctort  tlu'y  become  at  all  prominent.  The  patients  most  commonly 
noticed  them  from  two  to  five  years  before  death  :  but  in  some,  in  which 
tiie  disease,  from  the  ajjpearance  of  the  kidneys,  must  have  e.\iste<l  for 
many  years,  the  complaints  of  the  patients  did  not  commence  until  four 
to  live  months  before  their  end  (see  cases  28  and  29). 

In  practically  all  of  our  cases  the  history,  when  complete  enouj,di, 
contains  quite  definite  evidence  of  renal  disease,  with  the  one  exception 
of  case  30,  in  which  there  is  a  fairly  typical  history  of  gout,  but  other- 
wi-ic  nothing  suggesti\e  of  disease  of  the  kidneys  except  the  one  com- 
plaint that  he  had  to  urinate  frequently  and  had  to  get  up  several  times 
at  night.  Curiously  enough  in  this  case  the  urinary  findings  also  were 
very  slight:  both  in  si)ite  of  the  fact  that  the  lesions  in  the  kidneys  in 
the  gross  and  histologically  were  unusually  severe  (  see  fig.  59 ) . 

There  is  another  case  (  22 )  in  which  the  only  symptom  for  the  last 
three  years  before  death  was  occasional  nycturia.^  .\  rather  common 
initial  symyitom  was  oedema,  which  in  several  cases  commenced  in  the 
face,  but  not  so  rarel\  at  the  ankles.  The  time  of  onset  of  this  initial 
symptom  \aried  greatly. 

In  case  16  oedema  of  the  face  and  legs  developed  three  years  before 
death,  and  since  then  recurred  at  intervals.  Similarly  in  case  17  oedema 
and  dyspnoea  made  their  appearance  two  and  one-half  years  before  the 
end.  Facial  oedema  was  not  observed  until  considerably  later.  In 
[)atient  20  the  first  symptoms  manifested  themselves  four  years  before  he 
died,  and  consisted  of  general  oedema  and  ascites.  In  this  case  the 
oedema  disa])peared  comjiletely,  to  return  slightly  for  a  short  time  two 
months  before  death.  .Ml  that  was  left  eventually  was  some  puffiness 
about  the  eyes.  In  case  22,  as  stated  before,  the  only  symptom  for  several 
years  was  occasional  nycturia.  It  was  only  ciuite  late  in  the  disease  that 
he  developed  marked  oedema  of  the  lower  extremities,  with  very  marked 
dysjjuoea  and  cyanosis.  Case  24  started  in  with  dyspnoea  and  increasing 
weakness  two  years  before  his  death.  The  dyspnoea  again  was  a  prom- 
inent feature  in  his  last  attack  in  which  some  facial  oedema  was  ob- 
served ;  but  there  was  no  other  oedema  at  any  time.  Patient  26  became 
dropsical  as  early  as  five  years  before  his  death,  and  had  another  similar 
attack  four  years  later.  In  addition  he  complained  of  dyspnoea,  palpita- 
tion of  the  heart,  jjrecordial  pain,  headache  and  jjains  in  the  legs.  Patient 
2<)  had  noticed  puffiness  of  the  face,  swollen  legs,  shortness  of  breath, 
l)alpitation  of  the  heart,  and  precordial  |)ain  for  about  four  to  five  months. 


•■' Tlic  word  "nycluria"  in   this  paper  i.s  used   as  meaning   iiriii.iiinn  at   iiIkIu, 
and   is   not   meant   to  refer  t<)   involuntary   urination. 


26  Tlli'.    l'.\Til()l,(K;V    OF    NEPHRITIS 

There  is  no  history  of  a  previous  attack,  hut  the  data  are  incomplete.  In 
case  31  the  exact  nature  of  the  renal  symptoms  which  were  first  observed 
when  she  was  pregnant  five  years  before  death  is  not  stated;  but  in  her 
subsequent  history  oedema  is  not  a  very  prominent  symptom. 

In  six  cases,  then,  oedema  was  an  early  and  prominent  symptom. 

Dyspnoea,  as  may  be  seen  from  the  above,  was  often  noticed  very 
early,  and  this  symptom  frequently  was  very  severe,  out  of  all  proportion 
to  any  disturbance  in  circulation  that  might  have  been  present.  In  case 
28  it  was  an  early  and  apparently  the  most  prominent  clinical  symptom, 
not  associated  with  oedema  or  any  more  definite  "uraemic"  manifestation. 
It  is  not  at  all  improbable  that  the  attacks  of  "asthma"  in  case  19  which 
preceded  the  end  by  four  years  were  of  this  nature.  In  this  patient  it 
was  years  later  that  oedema  first  developed,  and  he  died,  similarly  to  case 
28,  in  extreme  dyspnoea. 

Palpitations  of  the  heart  were  quite  frequently  complained  of,  and 
in  a  few  instances  there  was  quite  a  little  precordial  distress,  sometimes 
suggesting  angina  pectoris.  The  patient  in  whom  this  symptom  was  most 
prominent  (17)  had  an  unusually  well  marked  general  arteriosclerosis. 
The  right  coronary  artery  was  almost  closed  at  one  point,  but  there  were 
no  scars  in  the  heart  muscle.  In  case  26,  with  similar  symptoms,  the 
necropsy  also  revealed  marked  arteriosclerosis  of  the  coronary  arteries. 
In  cases  21  and  29,  however,  in  which  anginoid  attacks  were  complained 
of,  there  were  no  lesions  in  the  coronary  arteries  or  in  the  heart  muscle, 
and  merely  a  few  small  yellow  spots  in  the  base  of  the  aorta.  (Jn  the 
other  hand,  in  case  18,  in  which  there  were  small  scars  in  the  musculature 
of  the  left  ventricle,  no  local  symptoms  were  complained  of.  Patient 
24,  in  whom  the  heart  muscle  was  similarly  atiected,  also  did  not  com- 
plain of  any  subjective  symptoms  in  the  region  of  the  heart,  but  clinical 
examination  revealed  an  absolute  arythmia.  ( It  may  be  stated  that  the 
heart  muscle,  like  all  other  important  organs,  was  examined  microscopic- 
ally in  all  cases. ) 

In  a  certain  number  of  cases  "uraemic"  symptoms  occurred  early 
and  often  dominated  the  clinical  picture.  In  the  early  stages  the  con- 
vulsive form  of  uraemia,  characterized  by  headache,  vomiting,,  and,  in 
extreme  cases,  convulsions,  was  usually  encountered.  Towards  the  end 
the  symptoms  of  true  uraemia  made  their  appearance,  often  terminating 
in  coma.""  In  case  17,  for  instance,  the  first  symptoms  two  years  before 
death  were  headache,  dizziness,  loss  of  memory,  failing  eyesight,  short- 
ness of  breath,  progressive  weakness,  and  frequent  urination.     This  man 


*  A   discussion   of   the   different    forms   of   uraemia   cannot   here   be   attempted, 
and  the  reader  is  referred  to  the  voluminous  literature  on  this  subject. 


ciiRoMi-  (■.i.umi:ki'i.(i-.\i:i'iihi IIS  27 

ni'Vi-r  li;ul  any  dfiicma.  i'xcc])l  slijjlu  i)iirtiiK'ss  of  tlu'  cvditls.  lie  liad  ;i 
retinitis  alhuminnrica.  iiraemic  convulsions,  and  died  in  coma.  TIk- 
symi>toiTis  of  patient  21  started  thirteen  years  before  her  death  with  in- 
tense headache  and  vomitintj.  She  liad  much  oedema  at  times,  and 
eventually  develo|)ed  symptoms  of  true  uraemia.  In  case  23  the  uraemic 
convulsions  were  cvidentlv  mistaken  for  ei)ik"])sy.  When  he  came  to  the 
hos]ntal.  he  comi>laineti  of  shortness  of  l)reath,  increasing  dimness  of 
vision,  cramps  in  the  legs,  and  deep  jiains  in  the  liones.  He  never  had  any 
oedema,  and  died  in  uraemic  coma. 

In  other  cases  again  the  uraemic  symptoms  were  a  late  develojiment. 
as  in  patient  20,  who  first  had  considerable  oedema.  Later  the  oedema 
was  much  less  marked,  but  he  had  intense  headaches  with  vomiting.  l)e- 
came  severely  dyspnoeic,  was  intensely  hyi)ersensitive  all  over  his  body, 
esjiecially  to  deep  pressure,  and  died  in  an  attack  of  excessive  dyspnoea. 
The  patient  (22)  in  whom  frequent  urination,  especially  at  night,  was 
the  only  symptom  for  several  years,  eventually  develo])ed  an  intense 
dyspnoea,  had  some  oedema,  and  died  in  uraemic  coma.  In  patient  31 
the  exact  symptoms  of  her  earlier  attacks  are  unfortunately  unknown. 
One  year  before  death  she  noticed  anorexia  and  vomiting.  Later  she  had 
some  attacks  of  violent  delirium,  associated  w-ith  complete  unconscious- 
ness. For  the  last  seven  months  she  had  headache,  much  vomiting,  jerk- 
ings  and  cramps  in  legs,  progressive  amaurosis,  and  at  times  oedema  of 
the  feet.  Ophthalmological  examination  showed  the  typical  picture  of  an 
albuminuric  retinitis.  Tlie  sxinjitoms  of  true  uraemia  contiiuied  to  her 
death. 

Retinitis  albuminurica  was  observed  in  the  above  mentioned  two  cases 
only.  In  case  23,  in  spite  of  the  failing  vision,  the  backgrounds  were 
normal.  The  retinal  arteries  were  slightly  tortuous,  and  the  disturbance 
may  have  been  due  to  this  patient's  severe  anaemia,  associated  with  arter- 
ial spasm. 

.\11  iiaticnts.  with  few  exce[)tions.  suffered  from  severe  anaemia. 
.\bout  half  the  normal  number  of  erythrocytes,  or  less,  and  a  correspond- 
ing decrease  in  haemoglobin,  was  observed  in  cases  17.  19.  20,  23.  24,  28, 
29,  30,  31.  In  several  of  these  cases  there  was  a  marked  anisocytosis. 
Associated  with  the  anaemia  there  was  frec|uently  observed  a  tendency  to 
bleeding  in  skin  and  mucous  membranes,  assuming  at  time-;  the  severity 
of  a  haemorrhagic  diathesis. 

The  temperature  was  either  normal  or  often  subnormal,  with  oc- 
casional rises  to  99-  or  99.5°  F.  The  pulse  rate  was  either  normal,  or  as 
in  case  29  rather  slow  (between  60  and  80).  but  in  c|uite  a  number  of 
cases  it  varied  considerablv,  and  occasionallv  rose  to   icxj  or  e\en   120. 


28  rill-.  :•  A  rii()i.()i;N-  oi-  xia-iiKiTis 

I'licsc  (listiirbanccs  in  pulse  and  temperature  are  ])r()lial)ly  due  to  tlie 
associated  septic  conditions,  it  is  of  some  interest  that  in  case  21.  in 
which  an  old  septic  infarct  iieavily  infected  with  influenza  bacilli  was 
found  in  the  spleen,  the  temjjerature  was  normal,  hut  the  pulse  rate 
varied  a  f^reat  deal  and  sometimes  rose  to  120. 

in  practically  all,  hut  more  especially  in  the  uraemic  cases,  the  tonjjue 
in  I  lie  last  sta5.!;es  of  the  disease  was  heavily  coated  and  the  breath  was 
loul.  In  some  of  them  a  severe  pseudomembranous  and  ulcerative  stoma- 
titis developed  eventually,  which  in  case  16  was  mistaken  for  ili])htheria, 
because  it  started  in  the  ref^jion  of  the  tonsils  and  gave  rise  to  the  forma- 
tion of  greyish  membranes.  The  lesions  usually,  however,  are  much  more 
widely  distributed  than  those  of  diphtheria,  involving  gums,  palate,  inner 
surface  of  cheeks,  lower  surface  of  tongue  and  floor  of  mouth,  etc.  The 
base  of  these  su])erficial  idcerations  is  either  exposed  and  then  greyish 
while,  due  to  the  necrosis  of  the  tissues;  or  it  is  covered  with  thick 
brownish  crusts.  The  condition  is  so  characteristic  that  one  might  speak 
of  it  as  a  "stomatitis  iii'.ii'mica."  These  lesions  are  usually  directly  due 
to  streptococcus  infcclioii  of  the  weakened  tissues. 

In  the  majority  of  the  chronic  cases  the  systolic  blood  pressure  was 
distinctly  elevated,  varying  from  i(m  to  250.  I'levations  to  200  and  more 
were  present  in  five  cases  (  17,  iiS,  22,  23,  2()|.  As  the  cases  are  arranged 
somewhat  according  to  the  .severity  of  the  lesions  in  the  kidneys,  it  is 
evident  from  the  figiu-es  that  the  amount  of  destruction  of  kidney  tissue 
in  itsilf  docs  not  control  this  ])henomenon.  In  fact,  there  are  more  cases 
with  low  pressures  and  small  hearts  among  the  cases  with  the  most  ex- 
tensive destruction  of  renal  tissue  than  among  those  with  less  destruction. 
The  patients  with  unusually  high  pressures  were  all  rather  strongly  built 
males  between  45  and  35.  Three  of  them  had  a  marked  general  arter- 
iosclerosis, one  had  fairly  normal, and  the  last  one  entirely  normal  arteries. 
(  )n  the  other  hand  some  of  the  cases  with  the  most  marked  and  extensive 
general  arteriosclerosis  had  low  |)ressnres  and  small  hearts.  One  gets 
the  impression,  thereffire,  that  the  pressure  is  forced  up  more  energetic- 
ally in  comjiaratively  vigorous  individuals,  when  the  disease  develops 
com])aratively  ra|)idly  and  leads  to  death  before  extreme  changes  have 
taken  i)lace  in  the  kidneys. 

The  cardiac  liypertroi)hy  is  evidently  caused  by  the  hypertension,  but 
it  is  b\  no  means  pro])ortionate  to  it.     The  largest  heart  (24)  was  found 

in  an  in(li\i(lnal  with  .1  bl 1  pressure  of  170,  which  on  rest  in  bed  came 

down  to  I  55.  (  )n  the  whole,  the  hypertro[>hy  of  the  heart  remains  within 
moderate  limits,  varying;  from  one  and  one-fourth  to  one  and  one-half 
times  normal  size  in  bulk.      The  hypertrophy  is  primarily  a  concentric 


ciiKo.vit   (if.oMicKii.o-Minikri  IS  29 

hy|)iTtr()|ihy  of  the  left  ventricle  (see  for  instance  cases  i'»  and  10  I.  foi- 
lowcfl  by  its  dilatation  and  later  sometimes  l)y  involvement  of  the  rijjfht 
heart;  but  the  cases  showing  mnch  dilatation  on  the  rij^ht  side  and 
marked  cyanotic  atrojihy  of  the  liver,  as  a  sij^n  of  chronic  passive  con- 
jjfestion  in  the  perijjheral  veins,  arc  c|uitc  small  in  number  (see  cases  19, 
2(),  2-j ) . 

Cases  with  low  pressure^  and  normal,  or  even  small,  hearts  arc  I)y 
no  means  rare,  cs|)ccially  in  very  chronic  cases  with  extreme  contraction 
of  the  kidneys  (  see  cases  25,  28,  29  and  2^2 ). 

The  relation  of  chronic  nephritis  to  g'out  is  af:(ain  brought  out  jirom- 
iTiently  by  our  series  of  cases.  f)nly  one  of  them  (30)  had  a  definite 
clinical  history  of  gouty  arthritis,  but  gouty  lesions  in  kidneys  and  else- 
where were  encountered  in  five  cases  (24,  26,  27,  29,  30),  without  a  sys- 
tematic search  in  every  instance.  It  is  reasonable  to  assume,  therefore, 
that  actually  the  incidence  was  greater  than  is  indicated  in  our  records. 
It  appears  especially  to  occur  in  the  very  chronic  cases  with  extreme  kid- 
ney lesions  (second  half  of  this  series).  The  recent  observations  of 
Denis  ''  that  in  healthy  individuals  an  excess  of  purins  is  rapidly  excreted, 
leaving  the  uric  acid  percentage  in  the  blood  undisturbed,  whereas  re- 
tention follows  early  in  cases  with  renal  insufficiency,  may  furnish  some 
clue  to  the  frequency  of  this  association. 

The  death  of  the  patients  was  either  the  result  of  terminal  infection, 
usually  broncho-pneumonia  (cases  16,  23,  24,  25,  27,  28,  29.  30 ),  or  of 
true  uraemia  (  17,  18,  19,  20,  21,  22,  26,  27,  28,  31  ).  In  the  latter  case 
the  patients  often  develofied  uraemic  coma,  but  some  showed  no  disturb- 
ance of  consciousness,  merely  excessive  dyspnoea  (  19,  20,  28). 

As  may  be  seen  from  the  table  of  summary  of  the  cases,  the  urinary 
findings  were  fairly  constant  in  all  cases.  Polyuria  was  a  very  jirominenl 
symptom,  occurring  at  one  time  or  another  in  seven  out  of  the  thirteen 
cases  in  which  anything  definite  is  known  of  the  urine.  This  was  com- 
monly associated  with  frecpient  urination  at  night  (nycturia).  The 
amount  of  urine  was  definitely  increased  in  about  one-half  of  the  cases. 
\n  three  the  quantity  is  designated  as  decreased.  The  sjjccific  gravity  was 
generally  low  (loio  and  less).  The  lowest  specific  gravity  (1002)  was 
found  in  the  most  acute  case  (16)  of  this  scries.  The  specific  gravity 
was  low,  not  only  in  the  cases  with  polyuria,  but  also  in  some  of  those 
with  a  decreased  amount  of  urine,  suggesting  hy()Osthenuria  (Schlayer). 
■~ec  cases  22,  23  and  24. ) 

With  few  exceptions  (  19,  29,  30 ),  the  urine  contained  much  albumin 


^  Denis,   "The   K(Tect   of   itiKcstcd    Piiriiis   on    the    L'ric    .Arid    Conlc-nl    of   the 
IJIood."    Jour,  nf  Biol.  Chcm..  IQI5,  NXIH,   147. 


30  THE    I'ATIUM.DCV    OF    NEI'IIKITIS 

I  at  least  a  heavy  cloud).  The  allnimimiria  was  moderate  in  cases  19  and 
29.  In  case  30  no  albumin  was  found,  but  the  patient  was  at  the  hospital 
for  a  short  time  and  there  is  record  of  one  examination  only. 

The  finding  of  casts  was  not  so  constant.  There  were  several  cases 
in  which  no  casts  were  found,  but  repeated  examination  usually  revealed 
showers  of  casts  once  in  a  while.  Frequent  examinations  of  the  urinary 
sediment  are  therefore  of  great  importance.  Leucocytes  and  erythro- 
cytes were  discovered  only  occasionally.  The  difficulty  of  finding  formed 
elements  in  the  urine  at  times  is  rather  astonishing,  because  in  sections 
of  these  kidneys  casts  are  always  fairly  numerous,  and  frequently  quite 
a  few  tubules  are  filled  with  blood  or  leucocytes  (see  protocols  of  indi- 
vidual cases).  It  may  be  that  in  these  later  stages  the  contents  of  the 
tubules  are  washed  out  less  easily  and  are  carried  down  only  when  there 
is  a  more  or  less  sudden  flood  of  urine. 

The  phenolsulphone-phthalein  test  was  employed  in  a  few  cases  only, 
many  of  them  dating  back  before  its  introduction.  In  every  instance  the 
excretion  was  distinctly  slowed.  In  case  26  there  was  no  excretion  in 
three  trials. 

The  gross  appearances  of  the  kidneys  varied  considerably,  except 
that  they  all  showed  evidences  of  contraction.  The  capsule  was  more  or 
less  thickened  and  adherent.  The  surface  of  the  kidneys  was  either 
smooth  or  granular,  or  full  of  large  irregular  scars,  more  or  less  lobu- 
lated,  according  to  the  distribution  of  the  newly  formed  connective  tissue.** 
The  color  was  frequently  mottled,  purple  and  grey,  or  in  other  cases  dark 
red,  in  others  again  quite  pale.  In  quite  a  few  cases  one  could  make  out 
small  petechial  haemorrhages.  The  number  of  them  varied  from  a  few 
to  a  great  many.  In  some  instances  the  color  of  the  organ  was  distinctly 
brown  on  account  of  an  abundant  deposit  of  haematogenous  pigment  in 
the  epithelium.  On  the  cut  surface  the  cortex  naturally  appeared  more  or 
less  contracted,  and  on  account  of  the  great  structural  alterations  the 
normal  markings  of  the  cortex  had  disappeared  to  a  great  extent.  If 
there  was  much  epithelial  degeneration,  opaque,  frequent  yellowish  spots 
were  seen  scattered  through  the  cortex.  The  arteries  on  the  cut  surface 
varied  greatly.  In  some  cases  they  were  distinctly  thickened,  in  others 
they  were  entirely  normal.  The  same  is  true  of  the  main  stems  of  the 
renal  arteries. 

Histologically  the  connecting  link  of  all  cases  was  the  inflammatory 
lesions  in  the  glomeruli  and  the  inflammatory  proliferation  and  eventual 
fibrosis  of  the  connective  tissue.    The  great  variety  of  lesions  encountered 


"  The  differences  are   well   shown   in   the   photographs   acconipanyiii.n   the   inili 
vidiial  cases.     Thev  are  all   taken   at   nearly   one-half  norm.al   size. 


riiud.vu    (;i.()Mi:i<i:.(i-.\i;i'iii<i  IIS  31 

is  well  ilhislral(.'(l  in  tin-  iiiiotumiiru^raiihs.  Slill  ihcy  all  show  llit  same 
pattern.  The  intlaminatory  character  of  these  lesions  is  naturally  most 
evident  in  the  more  acute  cases,  but  even  in  the  very  old  cases  typical 
subacute  lesions  may  be  encountered  in  some  of  the  t^lomcruli  (sec 
photomicrot;Tai)h  of  case  31  )  and  in  certain  jiarts  of  the  interstitial  tis- 
sue. Eventually  most  of  the  glomeruli  become  shrunken  and  fibrous. 
The  newly  formed  connective  tissue  also  becomes  more  and  more  fibrous 
and  the  neutrophilic  leucocytes  disappear  from  il.  Inil  cosin<)|)iiiIes  and 
"Mastzellen"  persist  for  a  lonaf  time. 

The  extent  of  the  epithelial  defeneration  varietl  very  much.  In 
some  cases  sjranular  and  fatty  defeneration  was  \ery  well  marked,  in 
others  there  was  hardly  any  evidence  of  it.  1  cannot  say  that  it  apjieared 
as  if  the  cases  with  much  epithelial  degeneration  were  more  likely  to 
develop  oedema,  as  has  been  suggested.  It  is  to  be  considered  that  the 
relation  of  the  oedema  to  the  epithelial  degeneration  may  be  the  opposite 
from  that  which  is  usually  assumed.  If  there  is  general  oedema  at 
the  time  of  death  involving  the  kidneys,  tiie  existence  of  this  oedema  in 
the  kidneys  may  very  well  favor  the  (level(j|)ment  of  degenerative  changes 
in  the  epithelium. 

Eventually  the  majority  of  the  tulmlcs  collai^se,  and  the  amount  of 
tissue  destruction  may  continue  to  an  astonishing  degree  before  death 
ensues.  In  those  cases  in  which  the  glomerular  involvement  and  the 
connective  tissue  develoj^ment  are  of  a  i)atchy  character  the  remaining 
comparatively  normal  glomeruli  and  tubules  often  show  evidences  of 
compensatory  hypertrophy.  These  latter  conditions,  however,  do  not 
seem  to  have  much  effect  on  the  clinical  picture.  The  developnunt  of 
numerous  small  cysts  is  quite  common  in  the  later  stages. 

Macteria  w-ere  found  in  the  tissues  in  one  early  case  only  (case  i')). 
It  w-as  the  most  acute  case  of  this  series,  a  case  in  wliich  there  existed  an 
infection  of  old  atheromatous  ulcers  with  diplostreptococci.  The  diplo- 
streptococci  were  found  in  many  caf)illarics.  and  a  few  outside  in  the 
inflamed  connective  tissue.  <  )nce  more,  no  bacteria  were  discovered  in 
the  diseased  glomeruli. 

This  same  case  had  acute  and  very  marked  lesions  in  the  arterioles, 
consisting  of  hyaline  thrombosis  which  in  some  ])laces  filled  the  arterioles 
com])letely,  in  others  formed  a  thick  layer  on  the  inner  surface  partly 
above,  i>artly  below  the  endothelium.  In  other  small  arteries  these  hyaline 
masses  had  been  partly  or  com])letely  organized,  giving  rise  eventually 
to  the  ]jicturc  of  a  cellular  endarteritis.  In  what  appeared  as  the  later 
stages  of  the  same  |)rocess  much  elastic  tissue  had  developed  in  tlu- 
thickened  intima,  in  such  a  way  that  eventually  an  appearance  was  pro- 


32  •ini'.  i'ATiiiiL(i(,\   I)]-  Mcniunis 

duccd  resc-mMiny  tliat  (Joscrihcd  b\-  Jores  as  characteristic  of  tlie  "func- 
tional" hyperplasia  of  the  intima  in  arteriosclerosis. 

In  case  i8  the  thrombotic  obstruction  of  some  of  the  arterioles  had 
given  rise  to  the  formation  of  many  microsco])ic  anaemic  necroses.  Both 
the  small  and  the  lartjcr  arteries  showed  a  ver\-  marked  thickening  of 
the  intima.  ]iartly  with  liypcrjilastic  development  of  the  elastic  tissue, 
partly  without.  Similarl\-  the  two  [jrocesses  were  mi.xed  in  case  17. 
In  case  20  the  arterial  changes  seem  to  be  old,  l>oth  in  arterioles  and  in 
the  larger  arteries,  and  we  find  much  elastic  tissue  in  both  places.  In 
case  22  some  small  arteries  show  "endarteritis,"  others  "arteriosclerosis." 
In  this  and  many  other  specimens  (see  individual  records)  one  finds  all 
transitional  stages  between  these  two  conditions. 

In  a  general  way  one  may  state  that  the  arterioles  in  the  kidney  are 
aiifected  in  all  cases,  but  that  even  in  the  oldest  and  most  severe  cases,  like 
cases  31  and  32,  the  larger  arteries  in  the  kidneys  and  elsewhere  may 
show  very  little  evidence  of  disease. 

It  appears  therefore  ill  advised  to  indulge  in  too  much  speculation  in 
regard  to  the  etiology  of  the  process  in  the  arteries  from  the  histological 
appearance  of  the  lesions,  and  I  believe  that  until  further  proof  to  the 
contrar}'  is  forthcoming  we  are  justified  in  assuming  that  the  changes  in 
the  arteries  in  these  diseased  kidneys  are  of  an  inflammatory  nature,  just 
as  the  rest  of  the  lesions.  This  interpretation  would  harmonize  very  well 
with  the  observation  that  in  the  small  arteries  at  least  the  proliferation  of 
the  intima  is  frequently  preceded  by  lateral  thrombosis,  bearing  in  mind 
the  fact  that  inflammation  of  the  arterial  wall  necessarily  would  favor 
thrombosis. 


In  conclusion  I  ma}-  be  permitted  to  add  a  few  general  statements. 
It  may  seem  as  if  this  were  hardly  warranted  on  account  of  the  small 
number  of  cases  studied:  and  there  certainly  would  be  justification  for 
criticism,  if  an  attempt  were  made  to  elaborate  a  complete  pathology  and 
symptomatology  of  chronic  nephritis  on  such  a  slender  basis.  On  this 
account  all  preceding  statements  have  been  worded  so  as  to  refer  to  the 
individual  cases  only.  But,  on  the  other  hand,  a  few  thoroughly  studied 
cases  may  give  .some  food  for  general  reflection. 

If  these  cases  teach  anything,  they  certainly  bring  out  very  clearly 
the  loose  association  which  e.xists  between  the  condition  in  the  kidneys 
and  a  number  of  other  phenomena  which  have  usually  been  rather  loosely 
described  as  "nephritic."  Terms  like  "nephritic"  oedema  or  "nephritic" 
hvpertension  cannot  fail  to  give  the  impression  that  the  oedema  or  the 


COXCl.L'SIONS  Jj 

liy]iertensioii  i1c])cik1  directly  dm  the  coiiditioii  of  tlie  kidneys.  Tn  my 
mind  nothing  could  be  further  from  the  truth.  These  conditions  are  fre- 
Cjuenliy  associated  with  nephritis,  but  the  kidneys  themselves  plav  no 
demonstrable  role  in  their  origin. 

This  will  be  perhaps  more  easily  conceded  in  case  of  the  oedema.  All 
attempts  at  explaining  the  oedema  on  the  basis  of  the  disease  in  the 
kidneys  have  failed,  and  as  a  matter  of  fact  a  cursory  study  of  these 
thirty-two  cases  will  show  that  there  is  no  one  element  in  the  pathology 
of  the  kidneys  with  which  the  oedema  could  be  connected.  Practically 
the  same  lesions  may  be  observed  in  the  kidneys  of  patients  which  were 
"water-logged"  long  and  often,  and  in  jjatients  who  had  oedema  rarely 
or  not  at  all.  One  may  object  that  the  anatomical  picture  of  the  kidney 
does  not  give  a  true  rejiresentation  of  its  functional  capacity,  and  that 
functional  tests  show  that  certain  functional  derangements  of  the  kidney 
are  apt  to  be  associated  with  oedema.  I  very  much  hesitate  to  express 
an  opinion  on  this  latter  point  on  account  of  lack  of  ex])erience  and 
knowledge:  but  this  much  is  certain,  that  in  these  functional  studies  it  is 
often  difficult  to  determine  what  is  cause  and  effect ;  and  there  is  cer- 
tainly no  unanimity  of  opinion  among  those  most  competent  to  judge  in 
questions  of  this  character.  But  a])art  from  all  such  controversies,  how 
much  easier  of  solution  does  the  whole  question  become  if  we  give  up 
this  idea  and  state  the  relation  somewhat  in  the  following  manner : 
The  agency  which  produces  the  nephritis  (certain  bacterial  toxins),  in 
addition  to  injuring  the  capillaries  in  the  kidneys  also  injures  them  else- 
where, and  this  produces  the  oedema. 

\\'e  need  only  to  think  of  the  word  "intlammation"  to  realize  that 
this  is  possible,  because  the  most  striking  effect  of  bacterial  toxins  in 
the  tissues  is  injury  to  the  capillaries.  Of  diffuse  injury  to  the  renal 
capillaries  (besides  the  characteristic  lesions  in  the  glomeruli),  we  have 
ample  evidence  in  the  acute  and  subacute  cases  of  the  disease.  The 
oedematous  swelling  of  the  kidneys  is  often  extreme,  and  the  extent  and 
imjjortance  of  this  oedema  seems  to  have  hardly  sufficiently  impressed 
itself  upon  anatomists  and  clinicians.  If  this  is  the  true  relation  of 
things,  we  can  understand  much  more  easily  why  the  relation  of  the 
nejjhritis  to  the  oedema  should  be  so  varying.  In  a  certain  case  the 
kidneys  may  be  damaged  very  severely,  but  the  capillaries  in  it  or  else- 
where much  less  so;  and  vice  versa.  Given  damaged  capillaries,  the 
factors  which  damage  them  additionally  or  which  in  other  ways  favor 
the  development  of  oedema  may  naturally  provoke  to  manifestation  a 
condition  which  may  be  more  or  less  latent,  or  aggravate  an  oedema 
that   is   already  plainly   in   existence.     The   damage   being   general,   the 


34  THE    PATHOLUliV    OF    NEPIIKITIS 

capillaries  in  the  delicate  structure  of  the  eye-lids  may  show  the  damage 
first ;  whereas  in  other  cases  the  oedema  may  first  show  in  places  where 
the  circidation  is  relatively  poor,  as  in  the  region  of  the  ankles. 

It  appears  to  me  that  an  assumption  like  the  one  made  above  clears 
away  innumerable  difficulties,  and  at  the  same  time  permits  the  utilization 
of  all  the  important  data  which  have  gradually  accumulated  as  a  result 
of  patient  clinical  investigation.  I  should  suggest,  therefore,  that  the 
term  "nephritic   oedema"  should  be  replaced  by  "'oedema  in  nephritis." 

The  same  way  with  "nephritic"  hypertension.  Here  also  the  loose- 
ness of  the  interrelation  of  this  phenomenon  to  the  disease  of  the  kidneys 
is  so  evident  that  it  does  not  need  special  emphasis ;  in  fact,  this  lack 
of  correlation  has  been  the  despair  of  all  those  who  have  attempted  its 
e.xplanation  scientifically.  It  appears  a  little  more  hazardous  to  ascribe 
these  differences  also  to  differences  in  the  action  of  the  causative  agent 
which  provokes  the  nephritis.  It  is  not  known  of  bacterial  toxins  that 
they  affect  the  tonus  of  the  arterioles,  and  yet,  whatever  causes  the  hy- 
pertension must  affect  them.  The  condition  of  the  large  arteries  is  im- 
material. An  increased  activity  of  the  heart  would  be  easily  compensated 
for  by  the  vasomotor  regulatory  mechanism ;  but  when  the  tonus  of  the 
arterioles  is  increased  the  vasomotor  regulation  breaks  down,  as  we 
know  in  the  case  of  adrenalin  and  pituitrin  hypertension,  probably  be- 
cause the  mechanism  works  by  means  of  the  arterioles  and  has  little  reflex 
control  over  the  heart  action.  If  it  could  be  shown  that  substances  pro- 
duced by  bacteria  directly  or  indirectly  had  a  pressor  action,  then  all 
difficulties  would  disappear,  as  in  the  similar  case  of  the  oedema.  Then 
one  would  be  able  to  understand  why  we  should  have  sometimes  early 
and  extreme  hypertension,  at  other  times  none  at  all.  If  we  make  the 
further  assumption  that  these  or  similar  substances  soinctiincs  do  not  only 
stimulate  the  arterial  wall  to  contraction, but  also  injure  it,  we  would  come 
much  nearer  to  the  solution  of  the  "arteriosclerosis"  problem :  in  fact  it 
might  lead  us  to  an  entirely  new  conception  of  the  etiology  of  arterio- 
sclerosis and  its  puzzling  relation  to  hypertension  and  nephritis,  because 
after  all  is  said  and  done  arteriosclerosis  and  arteriosclerotic  hyperten- 
sion have  some  intimate  relation  to  nephritis,  but  certainly  not  the  one 
usually  thought  of,  namely,  that  the  nephritis  is  the  primary  factor.  .\n 
assumption  like  the  one  mentioned  above  is  naturally  still  altogether  spec- 
ulative, and  it  will  take  much  work  to  get  close  enough  to  these  important 
problems  to  make  positive  statements ;  but,  whatever  the  relation  is,  1 
believe  it  may  be  positively  asserted  that  nephritis  and  hypertension  are 
not  related  to  one  another  as  cause  and  effect. 

Clinicians   have   alreadv   recognized   that   certain    forms  of   uraemia 


arc  not  iliie  lo  the  injury  to  kidney  tissue,  luit  to  other  factors.  The 
convulsive  form  of  uraemia  is,  for  instance,  ahtiost  certainly  ihie  to  dis- 
turbances in  the  cranial  cavity,  tiie  exact  nature  of  which  is  still  far  from 
beint;-  recognized:  and  similarly  it  may  be  with  other  forms  of  this 
protean  symi)tom-com|ilcx.  The  onlv  condition  in  which  we  have  good 
reason  to  believe  that  it  is  directly  the  consequence  of  ilestruclion  of 
kidney  tissue  is  what  clinicians  now  usually  speak  of  as  "true"  uraemia; 
and  in  this  condition  the  evidence  that  it  is  due  to  an  inefficiency  on  the 
part  of  the  kidneys  to  excrete  some  as  yet  tuiknown  substance  or  sub- 
stances has  been  accumulating  rapidly  in  the  last  years. 

In  regard  to  the  changes  in  the  cuiiif'osiliun  of  the  urine  and  its 
sediment  I  wish  to  emphasize  once  more,  as  has  been  done  often  enough 
before,  that  the  condition  of  the  urine  is  a  fairly  accurate  measure  of 
the  severity  of  the  disease  in  the  kidneys  at  a  given  time,  and  no  measure 
at  all  of  the  extent  of  the  damage  to  the  renal  tissue.  Polyuria  and 
hyi)osthenuria  more  particularly  point  to  serious  involvement  of  much 
kidney  tissue,  although  of  course  other  possible  factors  have  to  be  taken 
into  account.  The  records  also  bring  out  clearly  that  frequent  careful 
urinanalyses  arc  of  great  importance  in  the  clinical  recogniticju  ol  the 
disease. 

It  is  impossil)le  to  condense  the  result  of  these  observations  into  a 
few  phrases,  but  our  main  conclusions  might  be  formulated  as  follows : 

1.  Diffuse  glomerulo-nephrilis  is  a  disease  which  may  occur  in  acute, 
subacute,  or  chronic  form. 

2.  The  etiology  of  the  acute  and  subacute  forms  is  evidently  to  be 
found  in  bacterial  infection,  and  this  is  quite  probably  true  of  the  chronic 
form. 

3.  The  bacteria  concerned  are  commonly,  but  not  necessarily,  mem- 
bers of  the  streptococcus  family. 

4.  It  is  probable  that  the  continuance  of  the  disease  in  the  kidneys 
is  due  to  the  continuance  of  the  infection  in  some  often  more  or  less 
hidden  focus. 

5.  It  is  suggested  that  one  should  look  upon  the  oedema,  the  hyi)er- 
tension,  the  arteriosclerosis,  and  certain  uraemic  manifestations  merely 
as  being  frequently  associated  with  nephritis,  rather  than  as  being  directly 
dependent  upon  it. 

6.  It  is  quite  conceivable  that  these  manifestations  are  the  result  of 
the  fortuitous  action  upon  other  tissues  of  the  same  cause  which  injures 
the  kidneys. 


36  THE    l'ATHOLOi;V   OF    NKI'HRITIS 


RECORD  OF  CASES 

Case  I.     Old  focal  and  acute  diffuse  glomerulo-nephritis  in  man  of  52 

years,  with  chronic  diplostreptococcic  endocarditis. 

X\  II,  60. —  J.  K.,  strongh-  built,  emaciated  American  engineer,  52  years 
old. 

The  patient  had  had  occasional  attacks  of  sore  throat.  His  tirst 
definite  S3mptoms  were  observed  eight  years  before  death,  when  he  de- 
veloped palpitations  with  dyspnoea.  A  similar  attack  with  chills  and 
fever  was  observed  three  years  later.  Eight  months  before  death  he  had 
oedema  of  the  legs.  His  last  attack  began  four  months  before  his  death 
with  abdominal  cramps,  diarrhoea,  dyspnoea,  and  expectoration.  During 
this  last  attack  he  ran  an  irregular  septic  temperature.  Clinically  he 
showed  evidences  of  aortic  regurgitation.  There  was  marked  oedema  of 
the  legs  and  later  of  the  trunk,  and  symptoms  of  hydrothorax.  Towards 
the  end  oedema  and  hydrothorax  disappeared.  He  had  a  slight  anaemia 
(4,000,000  reds;  Hb.  60%),  no  leucocytosis  (3-10,000).  He  had  a  posi- 
tive Wassermann  reaction,  although  he  denied  lues  and  nothing  sugges- 
tive of  syphilis  was  found  at  autopsy.  Two  blood  cultures  were  nega- 
tive. Diplostreptococci  were  found  in  the  urine.  The  urine  showed  a 
heavy  cloud  of  albumin,  many  hxaline  and  granular  casts.  It  was  first 
decreased  in  amount,  later  increased  with  the  disappearance  of  the 
oedema.  The  phenolsulphone-phthalein  secretion  was  slowed  ( iS7o  ^'^^ 
hour,  15%  the  2d). 

Necropsy  revealed  an  old,  aortic  diplostreptococcic  endocarditis 
with  regurgitation,  and  a  large  spleen  with  numerous  large  areas  of 
haemorrhagic  softening  which  were  full  of  streptococci.  There  was  a 
slight  general  arteriosclerosis. 

The  kidneys  were  slightly  swollen  (12  x  6  x  3  cm.)  and  smooth. 
The  cortex  was  fairly  wide,  opaque,  and  showed  a  moderate  luimber  of 
haemorrhagic  spots.  There  was  a  small  anaemic  infarction  in  the  right 
kidney. 

Sections  showed  few  fibrous  glomeruli  with  areas  of  cellular  in- 
filtration and  moderate  thickening  of  the  connective  tissue  about  them ; 
few  neutrophilic  and  eosinophilic  leucocytes  in  these  areas  of  cellular 
infiltration ;  infiltration  of  most  glomeruli  with  neutrophilic  leucocytes ; 
recent  hvaline  necrosis  of  loops   in   a   fair  number :    no  extra-capillary 


I'lK-  I. 


38 


■iin-:  i'.\'iii(>i.n(,\-  i)\-  xicpHRiTis 


proliferation:  very  marked  liyperaemia  :  few  haemorrhages  ;  few  casts; 
little  epithelial  degeneration  ;  beginning  "arteriosclerosis"  of  some  small 
arteries.  Many  small  vessels  \yere  fillerl  with  coccus-emboli.  The  tissue 
ahmil  some  of  these  was  necrotic  and  showed  beginning  suppuration. 
No  cocci  were  found  in  am   of  the  diseased  glomeruli. 

Case  2.     Old  focal  and  acute  diffuse  glomerulo-nephritis  in  man  of  54 

years,  following  recrudescence  of  chronic  diplostreptococcic 

endocarditis. 

X\  II,  31. —  J.  N.,  American  kitchen-heliier,  54  years  of  agfc. 

Patient  had  an  attack  of  acute  [lolyarticular  rheumatism  followed 
b_\-  sharp  precordial  pain  radiating  into  arms  twenty  years  before  death. 
Since  th.en  he  had  had  three  to  four  attacks  a  vear.     He  was  alwavs 


WW 


short  of  breath,  and  had  |>alpitations  of  the  heart.  He  was  nervous  and 
slept  poorlw  At  times  he  had  severe  headaches,  dizziness  and  night 
sweats.  Lately  he  complained  of  renewed  ])ain  over  the  heart,  shortness 
of  breath,  and  oedema  at  the  ankles  which  he  observed  for  the  first  time. 
Clinically   he  presented  evidences   of  aortic  stenosis   and   regurgitation. 


Rr.coKi)  OK  CASKS  39 

Ili-s  blood  pressure  was  170  on  entrance,  Imt  later  went  down  to  140-150. 
lie  had  a  sli.yht  anaemia  (4,000.000  reds;  lib.  85%)  and  a  slight  Iciico- 
cvtosis  (  10,000).  He  had  a  positive  Wassermann  reaction,  although  he 
denied  lues;  nothing  suggestive  of  syphilis  was  found  at  autoi)sy.  His 
temiierature  was  at  times  subnormal,  and  his  jiulse  rate  varied  between 
80  and  100.  His  urine  showed  a  light  cloud  of  albumin  and  few  granu- 
lar casts. 

Necrops)'  revealed  an  old  aortic  diploslreptococcic  endocarditis  with 
recent  exacerbation,   moderate  general  arteriosclerosis. 

The  kidneys  were  of  about  normal  size  and  full  of  minute  haemor- 
rhages. 

Sections  showed  few  glomeruli  with  old  glomcrulo-nepiuilis  and 
^mall  areas  of  cellular  infiltration  and  connective  tissue  ])roliferation  in 
the  vicinity ;  infiltration  with  neutro])hilic  leucocytes  in  majority  of 
glomeruli;  necrotic  loops  in  few  of  them;  extra-ca))illary  proliferation 
about  some  of  these  tufts;  many  haemorrhages,  few  leucocytes,  few 
casts  in  tubules ;  marked  leucocytosis  in  capillaries  and  few  neutrophilic 
leucocytes  in  the  interstitial  tissue ;  marked  fatty  degeneration  and  bc- 
L^inning  necrosis  of  the  e])ithelium ;  beginning  "arteriosclerosis"  in  some 
-mall  arteries.     Xo  pathogenic  bacteria  were  found  in  the  sections. 

Case  3.      Old  focal  and  acute  diffuse  glomerulo-nephritis  in  a  man  of 

41  years,  with  old  diplostreptococcic  endocarditis. 
W  II.   188. —  M.  K.,  fairly  strongly  built,   fairly  well  nourished  Spanish 
farmhand  and  teamster.  41  years  of  age. 

History  imperfect  on  account  of  condition  of  ])atient.  who  died  one 
day  after  entrance.  He  claimed  to  have  been  well  until  a  sudden  break- 
down three  weeks  before,  while  at  work  in  the  fields.  Since  then  he 
became  weaker,  dyspnoeic  and  oedematous.  .\t  first  he  had  frequent 
urination  of  small  amounts  of  urine;  later  he  had  to  urinate  less  fre- 
(|uently,  and  the  oedematous  swelling  increased  correspondingly.  A  few 
days  before  death  he  began  to  have  bloody  expectoration.  Clinical  ex- 
amination showed  extreme  dysjinoca.  much  cough  with  bloody  expector- 
ation, a  heart  of  apiiarently  normal  size,  a  blowing  systolic  murmur, 
much  oedema.  He  had  a  high  pulse  rate  (103)  and  a  moderate  tempera- 
ture 101°  F).  His  blood-pressure  was  140.  His  urine  had  a  specific 
gravity  of  1012,  contained  much  albumin,  many  h\aline  and  granular 
casts,  and  few  leucocytes. 

Necropsy  revealed  an  old  aortic  dijilostreptoccic  endocarditis  witii 
some  stenosis,  a  heart  about  one  and  one-fourth  times  normal  size,  cyan- 


Fig.  4. 


Fig.  S. 


RKCORD   OK    CASKS  41 

Otic  atropliy  of  liver,  much  oedema,  ascites  and  hycirollioiax.  also  an 
acute  glaucoma  of  the  left  eye.     Tiie  arteries  were  practically  normal. 

The  kidneys  were  swollen  (13  .x  7  x  4J/  cm.)  and  smooth.  The 
cortex  was  wide,  yellow,  opaque,  and  full  of  minute  haemorrhages. 
There  was  an  old  infarct  in  the  left  kidney. 

Sections  showed  old  glomerulo-nephritis  in  few  glomeruli,  which 
were  surrounded  by  small  areas  of  cellular  infiltration,  and  librous  thick- 
ening of  the  connective  tissue.  The  majority  of  the  glomeruli  were  in- 
filtrated with  neutrophilic  leucocytes :  hyaline  necroses  were  found  in 
several,  and  beginning  extra-capillary  i)ro]iferation  in  some.  Some 
tubules  were  filled  with  blood :  many  also  contained  leucocytes.  The 
interstitial  tissue  was  moderately  infiltrated  with  neutrophiles.  There 
was  little  degeneration  in  the  e])ithelium :  beginning  "arteriosclerosis"  in 
few  small  arteries.  The  sections  were  loo  badly  contaminated  to  permit 
of  bacterioloijical  examination. 


Case  4.     Acute  glomerulo-nephritis  in  woman  of  33  years,  with  cir- 
rhosis and  large  septic  phagedenic  ulcers  of  leg. 
X\lll.   138. —  Mrs.  A.   1!.,  delicately  built,   fairly  well  nourished   Italian 
housewife,  33  years  of  age. 

I'atient  came  to  clinic  two  years  before  death.  ci;niplaining  of  swell- 
ing of  abdomen  and  feet.  Five  years  before  death  she  had  her  first 
attack  of  swelling  of  the  abdomen  with  jaundice.  About  three  months 
before  death  ulcers  developed  on  the  right  leg,  which  became  |)rogress- 
ively  worse.  One  month  before  death  the  symjjtoms  of  cirrhosis  became 
more  aggravated.  Clinical  examination  showed  the  usual  symptoms  of 
cirrhosis,  large  phagedenic  idcers  on  right  leg.  Treatment  with  salvar- 
san  made  the  ulcers  on  the  legs  much  worse.  1  ler  temperature  was  high 
and  somewhat  irregular:  her  pulse  accelerated  and  irregular.  Towards 
the  end  she  became  irrational,  and  some  oedema  appeared  on  her  face. 
The  W'assermann  reaction,  which  had  been  negative  before,  became  posi- 
tive at  this  time.  She  was  tjuite  anaemic  (lib.  637c)-  The  urine  con- 
tained much  albumin,  at  times  many  granular  and  cellular  casts,  and  very 
many  leucocytes. 

Necropsy  revealed  extensive  old  cirrhosis  and  several  large  phage- 
denic ulcers  on  right  leg.  Smears  from  the  most  acute  one  of  these 
ulcers  showed  many  streptococci.  Streptococci  were  also  found  in  a 
thrombus  in  the  right  auricle  and  in  the  spleen.  The  heart  was  slightly 
dilated  on  the  right  side.    The  large  blood-vessels  were  normal. 


42 


THE   PATHOLOC.V   OF    NEPHRITIS 


The  capsule  of  the  kidneys  stripped  easily.  The  surface  was  very 
slightly  granular.  They  v\'ere  extremely  hyperaemic  and  oedematous, 
and  very  distinctly  swollen  (12JX  x  6  x  43^  cm.).  On  the  cut  surface 
the  cortex  was  wide,  and  showed  a  certain  number  of  small  opaque  spots. 
No  haemorrhages  were  seen  in  the  gross  specimen. 

Microscopic  sections  showed  a  diffuse  intra-capillary.  and  in  places 
extra-capillary,    giomerulo-nephritis.      The    glomeruli    were    heavily    in- 


filtrated with  polymorphonuclear  leucocytes.  Many  of  them  showed 
hyaline  necrosis  of  some  of  the  loops.  In  few  glomeruli  the  changes 
were  advanced  to  the  subacute  stage.  Many  tubules  were  filled  with 
blood  and  leucocytes.  The  eiiithelium  showed  some  granular  and  a  little 
fatty  degeneration.  The  interstitial  tissue  was  hyperaemic,  oedematous, 
and  slightly  proliferated.  There  was  a  moderate  infiltration,  with  gran- 
ular leucocytes  and  lymphocytes.  \o  bacteria  were  found  in  sections. 
The  small  arteries  were  normal,  the  larger  ones  were  slightly  "arterio- 
sclerotic." 


RKCORP  OF    CASES 


43 


Case  5.     Early  subacute  glomerulo-nephritis  in  a  woman  of  33  years 

with  subacute  diplostreptococcic  endocarditis. 
XX'III,  166. —  Mrs.  K.  11.,  .stroiiLjly  built,  jioorly  nourisla-d  llalian  liou.sc- 
wife,  33  years  of  age. 
Patient  was  admitted  to  hospital  ten  days  before  her  ilealh,  com- 
plaining of  vomiting,  shortness  of  breath,  and  swelling  of  feet.  Nine 
months  liefore,  she  had  an  attack  of  acute  ])olyarticnlar  rheumatism, 
ushered   in   by   tonsillitis.      The   ])ains   in    die    joints    continued    intermit- 


tently for  about  >ix  months.  Ten  weeks  before  admission  her  stomach 
trouble  began,  and  she  vomited  fre(|uently.  I  ler  d\  si)noea  .started  six 
weeks  later,  and  the  oedema  commenced  one  week  before  entrance. 
Clinical  examination  showed  marked  dyspnoea,  slight  icterus,  coateil 
tongue,  an  enlargement  of  the  heart  lo  the  left,  a  systolic  blowing  murmur 
at  the  apex,  transmitted  to  axilla  and  back,  also  a  i)resytolic  murmur, 
marked  general  cyanosis  and  oedema.  ])etechial  haemorrhages  in  skin 
and  mucous  membranes.  The  patient  vomited  very  much,  was  very 
restless  at  times,  at  others  drowsy,  had  some  muscular  twitchings  in  face, 
and  died  of  gradual  circulatory  failure.  She  was  distinctly  anaemic 
(3,392,000   reds;    48^     lib.).      There    was   some   leucocytosis    (12.740). 


Fig.  9. 


KIKOKII   OK    CASKS  45 

Diploslrcptococci  were  olitaincd  in  blood  culture.  I  Ur  liluod  pressure 
was  loo.  The  temperature  was  sulinorinal.  witli  ele\ations  to  99^  !■'. 
The  pulse  rate  varied  between  So  and  100.  The  urine  contained  much 
albumin,  many  hyaline,  "granular  an<l  cellular  casts,  manv  leucoc\tcs  and 
much  blond,  also  diplnstrei)tococci. 

XecropsN  revealed  subacute  diplostre|)tococcic  endocarditis  of  mitral 
.111(1  iricuspicl  \alves.  embolic  septic  foci  in  heart-muscle,  infarcts  in 
s|»lcen  and  kidney,  septic  necroses  in  liver,  cholelithiasis,  and  terminal 
broncho-pneumonia.  'J"he  heart  was  moderately  enlartjed  on  the  rig^ht 
side  on  account  of  mitral  disease.     The  blood-vessels  were  normal. 

The  kidneys  were  swollen  f  1 1  ^  x  6^  .x  4  cm. :  1 2  .\  7  .\  5  respcct- 
ivelxi.  The  capsules  stripped  easily.  The  surface  was  smooth,  dark 
greyish  red.  and  studded  with  minute  haemorrha,u;es.  On  the  cut  surface 
the  corte.x  was  wide,  distinctly  oedematous.  and  greyish  red. 

Microscopic  sections  showed  diffuse  acute  and  subacute  glomcrulo- 
n('|ihritis  (intra-  and  e.xtra-capillary  )  :  much  blood  and  m;mv  leucocytes 
in  tubules,  many  ncutro])hilic  leucocytes  in  glomeruli  and  in  interstitial 
tissue,  few  eosino])hiles  and  basoi)hiles,  comj^aratively  little  epithelial  de- 
generation, and  beginning  proliferation  of  the  connective  tissue:  arter- 
ies normal.  \'o  bacteria  were  found  in  sections,  in  spile  of  careful 
M-arch. 

Case  6.      Early  subacute  glomerulo-nephritis  in  an   infant  with  con- 
genital syphilis  and  suppurative  colon-bacillus  pyelitis. 
.\\  1,  50. —  .\.  C,  anaemic  female  child,  i ,' _>  months  of  age. 

The  child  was  apparently  normal  at  birth,  was  sick  for  about  two 
weeks  with  sanguino-purulent  discharge  from  nose,  and  fever  to  101'  F. 
.Several  blisters  developed  on  abdomen.  .\t  the  hosi)ital  occurred  a  more 
general  eru])tion  of  red  blisters.  The  hands  were  oedematous  on  en- 
trance, but  the  oedema  disajipcarcd  later.  Moist  rales  were  heard  over 
the  lungs.  The  W'assermann  reaction  was  positive.  A  heavy  cloud  of 
albumin  was  found  in  the  urine,  a  few  doubtful  hyaline  casts,  and  many 
leucocytes.    Patient  died  in  collapse  witii  symptoms  of  pulmonary  oedema. 

.\'ecro])sy  revealed  syphilitic  rhagades  at  mouth,  syphilitic  pneinnonia 
,tnd  subacute  septic  pneumonia,  syphilitic  cirrliosis  and  miliary  syphil- 
omata  of  the  liver,  subacute  dcej)  idcerative  infection  of  renal  jielvis 
with  colon-bacilli  and  beginning  involvement  of  kidneys.  The  arteries 
were  normal. 

The  kidneys  were  large.      The  cortex  was  o|)ar|ue  and  swollen. 

Sections  showed  hyaline  necrosis  of  vascular  loops  in  the  majority 
of   the   glomeruli,   with   subacute  glomerulitis    (extra-capillary).      Many 


46 


rin-;  patiiolocv  oi-"  nepiikiti;- 


tubules  were  filled  with   lilciod,  others  contained  leucocytes.     There  was 
a  marked  infiltration  of  the  interstitial  tissue  with  nculroiiliilic.  eosino- 


philic leucocytes  and  plasma  cells,  and  cellular  proliferation  of  the  con- 
nective tissue.  The  \essels  were  normal.  Xo  bacteria  were  found  in 
the  sections,  excejit  at  the  evidently  infected  places. 


Case  7.     Subacute  glomerulo-nephritis  in  a  man  of  40  years,  following 

subacute  endocarditis. 
XVII,  163. —  E.  G.,  dishwasher,  40  years  of  age. 

Patient  had  a  paralytic  stroke  associated  with  left-sided  hemijilegia 
and  sensory  aphasia  seven  months  before  death.  He  had  a  chancre  two 
years  before,  and  at  the  time  he  came  to  the  hospital  had  a  |>ositive 
Wassermann  reaction.  Clinically  he  showed  a  systolic  murmur  at  the 
apex,  general  oedema,  some  anaemia  (4,800,000  reds,  85%  Hb.).  and 
slight  leucocytosis  (11,200).  He  had  an  irregular  temperature  varying 
between  96°  and  102°  F.  His  ])ulse  rate  varied  between  70  and  100.  His 
urine  contained  a  moderate  amount  of  albumin  and  a  few  hyaline  casts. 

Necropsy  revealed  a  subacute  diplostreptococcic  endocarditis  of  the 
mitral  valve,  with  regurgitation,  an  embolic  softening  in   the  region   of 


iHl)   Ol'    CASKS 


47 


the  right  island  of  Keil.  a  hci^iiinin:;  cyanotic  alrojjhy  of  tin-  li\ir.  •jcii- 
eral  oedema,  marked  h\drothora.\  and  normal  arteries. 

The  kidneys  were  swollen:    the  corte.x  was  rather  wide  an<l  i)|)a(|ue, 
and  full  of  jietechiai  haemorrhages. 


Secticjns  showed  hyaline  necroses  in  many  glomeruli,  tvpical  diliuse 
subacute  and  more  chronic  glomerulo-nephritis  ( intra-  and  e.\tra-cap- 
illary  i  :  moderate  diffuse  cellular  thickening  of  the  connective  tissue,  in 
which  there  were  (|uite  a  few  neutro|)hilic  and  less  numerous  eosino])hilic 
and  basophilic  leucocytes:  marked  hyperaemia :  Mood  antl  leucocytes  in 
many  tubules:  much  epithelial  degeneration:  normal  blood-vessels.  Xo 
pathogenic  b:icleria  were   found  in  llie  sections. 

Case  8.     Marked  subacute  glomerulo-nephritis  in  a  man  of  45  years, 

following  streptococcic  infection  of  compound  fracture. 

.\l\  .   :!4. —  I.  \\'.,  slrongK  built.  luuscular  .American  carpenter.  45  years 

old. 

Patient  had  a  compound   fracture  of  the  left  leg  ei.yht  and  o:ie-lialf 

months  before  death.     The  bones  became  united,  but  the  wound  never 

(|uite  healed  and  later  broke  ojien.  leaving  a  constantly  discharging  ulcer 


48 


THE   P.\TII()1.0(;^•    OK    NEPHRITIS 


from  which  a  small  piece  of  necrotic  bone  came  away  at  one  time.  Many 
streptococci  were  found  in  the  infected  tissues.  The  temperature  was 
normal   most  of  the  time,  but  there  were  sharp  rises  off  and  on.      His 


urine  was  smoky,  contained  much  albumin,  many  h\aline  and  waxy  casts. 
many  red  cells. 

X'ecropsy  revealed,  in  addition  to  the  infected  fracture,  a  marked 
anaemia  and  broncho-pneumonia,  possibly  a  slight  hypertrophy  of  the  left 
ventricle,  slight  oedema  of  leg,  slight  general  arteriosclerosis. 

The  kidneys  were  somewhat  swollen  (  12  x  7  x  4  cm.).  The  surface 
was  smooth,  mottled  grey  and  red.  The  cortex  was  wide,  hyperaemic 
and  oedematous,  and  full  of  minute  haemorrhages. 

Sections  showed  hyaline  necrosis  in  vascular  loops  of  many  glom- 
eruli; very  characteristic  acute  and  subacute  glomerulo-nephritis  (extra- 
capillary) in  i)ractically  all;  moderate  diffuse  infiltration  of  interstitial 
tissue  with  neutrophiles,.  eosinophiles,  basophiles,  and  marked  diffuse 
fibrous  thickening  of  the  connective  tissue.  Many  tubules  were  filled 
w4th  blood,  others  with  leucocytes.  The  epithelium  showed  much  fatty 
degeneration.  Slight  "arteriosclerosis"  in  a  few  of  the  larger  arteries. 
A  few  doubtful  diplococci  were  found  in  the  diseased  glomeruli  and  in 
the  leucocvtes  in  some  of  the  tubules. 


RIXORD   OF    CASliS 


49 


Case  g.    Subacute  glomerulo-nephritis  in  a  man  of  33  years,  following 

subacute  diplostreptococcic  endocarditis. 
X\  .  i_^5. —  H.  D.,  stronijly  Wuilt.  ciiiaciatcil,  AnuTicaii  iiospital  (irdi'rJN-, 
33  years  of  age. 
Patient  infected  his  finger  eight  months  before  his  death.  The  in- 
fection was  followed  by  chills  and  fever,  increasing  weakness,  and  grad- 
ual development  of  symptoms  of  septic  endocarditis,  with  remittent  fever 
and  progressive  anaemia  (eventually  3.800,000  reds;  56':;  Mb.,  5,000 
leucocvtes,  and  occasional  mvcloc\tes  ).     Three  months  before  his  death 


patient  noticed  oedema  at  ankles,  increased  thirst,  and  increased  urina- 
tion. Since  this  time  he  compla.ined  of  headaches  and  dyspnoea.  The 
W'assermann  reaction  was  negative.  Blood  cultures  were  negative  on 
two  occasions.  His  urine  was  increased  in  quantity  (specific  gravity 
1010-1016),  showing  a  heavy  cloud  of  albumin  (about  0.5%),  many 
hyaline  and  granular  casts,  a  moderate  number  of  leucocytes,  and  at  times 
many  red  cells.  Phenolsulphone-phihalein  excretion  two  weeks  before 
death  :   40%  in  two  hours. 

Necropsy  revealed  a  subacute  aortic  di])lostreptococcic  endocarditis 
with  moderate  stenosis  and  some  insufficiency,  a  purulent  mcdiastinilis. 


50  THE   PATHOI.OCV    OF    .NEI-HRITIS 

and  a  fibrinous  pleurisy,  both  due  to  the  diplostreptococci,  a  large  spleen 
with  a  septic  infarction,  no  oedema,  normal  arteries. 

The  kidneys  were  of  about  normal  size ;  the  surface  was  smooth. 
The  cortex  was  wide,  opaque,  intensely  hyperaemic,  and  full  of  haemor- 
rhages. 

Sections  showed  hyaline  necrosis  of  loops  in  many  glomeruli,  very 
typical  subacute  glomerulo-nephritis  ( intra-capillaryj  in  practically  all, 
large  areas  of  cellular  infiltration  (containing  neutrophilic  leucocytes), 
and  much  fibrous  thickening  of  the  connective  tissue,  with  beginning 
atrophy  of  the  tubules.  Some  tubules  were  full  of  blood,  others  con- 
tained casts.  Much  granular  and  fatty  degeneration  was  found  in  the 
epithelium,  also  extensive  necrosis.  Normal  blood-vessels.  No  patho- 
genic bacteria  were  found  in  sections. 

Case  10.     Subacute  glomerulo-nephritis  with  continued  hypertension 

and  cardiac  oedema  in  woman  of  27  years,  following  abscess 

of  jaw. 

X\TII,  106. —  M.  O.  A.,  poorly  nourished  Spanish  housewife,  2~  years 
old. 

Twenty-one  months  before  death,  patient  had  considerable  trouble 
with  her  teeth,  lasting  for  eight  months :  finally  alveolar  abscess  devel- 
oped, and  one  tooth  had  to  be  removed.  This  abscess  involved  lower  jaw, 
and  had  to  be  drained  from  outside.  She  had  been  apparently  well  since 
then,  until  four  weeks  before  her  death,  when  she  developed  a  painless 
oedema  of  the  legs,  without  an}-  other  symptoms.  The  swelling  con- 
tinued, and  the  abdomen  also  became  involved.  Ten  days  before  death, 
symptoms  of  an  acute  infection  developed  in  the  right  leg.  She  developed 
an  irregular  fever  to  102°  F;  her  pulse  rate  varied  l)etween  lOO  and  140. 
There  was  also  some  leucocytosis  (  10-15,000).  Clinically  there  were  no 
important  findings  except  oedema  and  evidences  of  cellulitis.  Her  haemo- 
globin was  8o7c,  her  blood  pressure  160.  gradually  rising  to  170.  Her 
urine  was  quite  scanty,  specific  gravity  loio:  it  contained  much  albumin, 
many  hyaline  and  granular  casts,  many  red  and  white  cells.  She  had  no 
symptoms  of  uraemia,  and  died  of  the  acute  strejjtococcic  infection  of 
her  leg. 

Necropsy  revealed  streptococcic  cellulitis  of  the  right  leg,  broncho- 
imeumonia,  some  ascites  fa  pint  of  fluid),  and  an  acute  cystitis.  Her 
left  ventricle  was  slightly  hypertrophied.  There  was  no  arteriosclerosis 
except  in  the  renal  arteries,  where  it  was  of  a  moderate  degree. 


THI-;   PATHOLOGY    OF   NEPHRITIS 


Her  kidneys  were  of  about  normal  size  (12  x  5  x  4  cm. )  :  the  cap- 
sule was  slightly  adherent ;  the  surface  slightly  roughened.  The  cortex 
was  rather  wide,  yellow,  and  opaque. 

Microscopical  sections  showed  subacute,  peri-capillary  glomerulo- 
ne])hritis  in  many  glomeruli,  with  development  of  fibrous  connective  tis- 
sue between  ca])illaries,  hyaline  degeneration  of  the  wall  of  some  of  the 


ca])illaries  in  the  tufts,  moderate  diffuse  thickening  of  the  connective  tis- 
sue with  beginning  atrophy  of  some  of  the  tubules,  leucocytes  in  manv 
tubules,  many  hyaline  casts,  no  haemorrhages,  and  much  epithelial  de- 
generation. The  thickened  interstitial  tissue  is  almost  altogether  fibrous. 
There  are  very  few  small  areas  of  lymphocytic  infiltration  ;  no  granular 
leucocytes  were  found  in  the  tissues.  Xo  bacteria  were  found  in  the 
sections,  in  spite  of  continued  search. 

Case  II.     Late  subacute  glomerulo-nephritis  in  a  man  of  51  years,  fol- 
lowing chronie  diplostreptococcic  endocarditis. 

X\'II,  119. —  M.  A.,  well  nourished  Norwegian  male  cook,  51   years  of 
age. 
Patient  began  to   complain  of  heart  trouble   four  years  before  his 
death.     He  had  had  some  oedema.     He  came  to  the  hos])ital  about  six 


RirCORD   OF    CASKS 


53 


weeks  bi'tore  death,  complaiiiim;  of  vomiting  and  dyspnoea.  Clinically, 
lie  showed  evidence  of  an  enlargement  of  the  heart,  and  a  marked  dias- 
tolic murmur,  also  symptoms  of  aortic  aneurysm.  The  hackgrounds  of 
his  eyes  were  normal:  there  was  no  definite  evidence  of  uraemia.  His 
temperature  was  subnormal  and  slightly  irregular.  His  ])ulse  rate  varied 
between  90  and  r>).  ilis  blood  showed  a  secondary  anaemia  (3,312,000 
reds,  6o</(  Hb.  1  and  a  lcuco])enia  (6200).  He  had  a  syjihilitic  history 
and    a   jiositive    W'assermann    reaction.      Ilis    blood    jiressure,    gradually 


rising,  varied  from  i.So  to  220.  .'^incc  over  onc-balf  year  before  death. 
he  had  noticed  polyuria  u\>  to  one  gallon  a  day.  The  ])olyuria  continued 
while  he  was  at  the  hospital.  Ilis  urine  contained  much  albumin,  many 
epithelial  and  granular  casts,  a  few  leucocytes,  occasionally  many  red 
cells.  It  had  a  low  sjjecific  gravity  (  1005-1010).  There  was  jjractically 
no  elimination  of  i)henolsidphone-|)hthalein  in  three  successive  tests. 

.\ecro])sy  revealed  sy])hilis  of  the  aorta  and  an  aneurysm  of  the  arch  : 
a  chronic  diplostre])tococcic  endocarditis  on  the  ventricular  side  of  the 
large  sail  of  the  mitral  valve  and  of  the  aortic  valves  with  little  ileformity 
of  the  aortic  cusps,  and  acute  dijilostreptococcic  jiericarditis,  slight 
ascites,  and  moderate  hydrothora.x  ;    old  cyanotic  atrophy  of  liver:    be- 


54  Till'.  j'.\iiioi.()i;v  oi-  Ni:i'iiRiTi.s 

ginnint;  amvloid  degeneration  of  t!ie  spleen,  no  amyloid  in  the  kidneys. 
The  heart  was  twice  normal  size,  with  a  very  marked  hypertroi)hy  of  the 
left  ventricle.    The  renal  and  splenic  arteries  were  markedly  sclerotic. 

The  kidneys  were  slightly  enlarged  (  13  x  7  x  4  cm.),  the  surface 
was  somewhat  rough,  dark  red,  and  full  of  haemorrhages.  On  the  cut 
surface  the  cortex  appeared  slightly  reduced  and  opaque. 

Sections  showed  very  marked  diffuse,  chronic,  subacute  and  acute 
glomerulo-nephritis  (intra-  and  peri-capillary),  with  hyaline  necrosis  of 
many  vascular  loops,  fibrin  in  capsules  of  many  glomeruli,  much  infiltra- 
tion with  granular  leucocytes,  especially  with  eosinophiles,  and  marked 
diffuse  thickening  of  the  connective  tissue  with  atrophy  of  many  tubules : 
blood,  leucocytes,  and  casts  in  tubules:  much  granular  degeneration  and 
necrosis  of  the  epithelium :  slight  "arteriosclerosis"  of  a  few  of  the  small 
arteries  and  several  of  the  larger  ones.  No  bacteria  were  found  in  sec- 
tions. 

Case   12.     Late  subacute  glomerulo-nephritis  in  woman  of  26  years 

with   repeated  attacks  of  tonsillitis,   a   general  diplostrepto- 

coccic  sepsis  with    infection    of   the    urinary   tract, 

multiple  thrombotic  arterial  obstruction. 

Will,  Oi. —  E.  AI.,  frail  and  extremely  emaciated  Irish-American  house- 
wife, 26  years  of  age. 
Patient  had  numerous  attacks  of  tonsillitis  from  infancy  to  four 
years  before  death.  She  was  treated  six  years  before  death  for  nephritis 
following  miscarriage.  I"or  the  last  five  years  she  had  much  headache, 
associated  with  vomiting.  Occasionally  she  had  slight  oedema  of  feet 
and  ankles.  I'our  months  before  death  she  complained  of  marked  weak- 
ness, headaches  associated  with  vomiting,  pains  in  shoulders  and  arms, 
loss  of  ])ower  in  left  arm.  She  bled  easily  from  her  mucous  membranes. 
Left  foot  had  been  cyanotic  in  region  of  big  toe  during  cold  spells  for 
the  past  two  years  ;  she  also  had  attacks  of  syncope  in  her  fingers.  Her 
eyesight  began  to  fail  at  this  time.  When  she  entered  the  hospital  a 
month  before  death,  the  toes  of  the  left  foot  were  cold  and  blue  and  hor 
left  arm  contracted  and  atrophied.  Later  she  developed  dry  gangrene  of 
the  left  foot.  Her  tongue  was  dry  and  red.  her  breath  uraemic.  The  heart 
action  was  heaving.  There  was  a  slight  systolic  and  diastolic  murmur. 
and  considerable  ascites.  .  She  later  developed  some  oedema  of  the  legs. 
Towards  the  end  there  was  marked  pufffness  of  the  face.  She  had 
been  complaining  of  failing  eyesight  for  some  time,  and  ophthalmoscopic 
examination  revealed  retinitis  albuminurica.     Shortlv  before  her  death. 


Ki:C()RU   OF    C.\S12S 


55 


slie  had  protusf  liainiorrliaj^cs  from  the  rectum.  Slic  died  in  uraemic 
coma.  Iler  temperature  was  irreguhir,  sliovvins;'  aUcniatiug  periods  of 
slight  rises  to  1 00°  I-",  and  of  sulmormal  temperature.  Iler  pulse  rate 
was  very  irregular,  varying-  between  Xo  and  130.  She  was  very  anaemic 
(Hb.  50%,  3,000,000  red>i.  Iler  leucocytes  were  normal  except  for  a 
terminal  leucocytosis.  In  a  Mcod  culture  a  pin-e  growth  of  dipiostrepto- 
cocci  was  obtained:  similar  organisms  were  found  in  her  urine.  She 
denied  all  venereal  infection,  and  had  a  negati\e  W  assermann  reaction. 
Iler  lilood  pressure  was  iC)5  cm  entrance,  went  up  to  1S5,  and  then  grad- 


#    A 


^^■ 


uall_\-  dfiwn  to  140.  She  had  hafl  nocturia  '  for  the  last  ten  years.  Iler 
urine  was  of  about  normal  amoinu,  of  low  specific  gravity  (1004-iOoSi. 
It  contained  nuuii  albimnin,  sometimes  few,  at  other  times  many  casts  of 
various  kinds,  some  red  blood  corpuscles  and  leucocytes.  Towards  the 
end  there  was  much  pus  in  the  urine.  The  i)henolsulphone-phthalcin 
secretion  was  much  delayed  (12%  in  two  hours  1. 

Necropsy  revealed  slight  oedema  of  hands  and  legs,  marked  ascites. 
The  ai)pendix  was  surrounded  by  old  adhesions.     There  was  also  some 

"  Urination   at   night. 


Fig.   19- 


RIXORD   OF    CASES  57 

peritoneal  thickening  in  the  upper  jiart  of  the  ahdoniinal  cavity.  The 
liver  showed  an  old  cyanotic  atrophy.  A  large,  deep,  recent  ulceration 
evidently  due  to  arterial  obstruction  was  found  in  the  sigmoid  tlexurc. 
The  heart  was  of  normal  size:  the  left  ventricle  firm,  full  of  small  irreg- 
ular necrotic  spots,  due  to  obstruction  of  small  arteries.  There  were  a 
few  small  yellow  sjjots  in  the  aorta.  The  renal  pelves  were  slightly 
dilated.  They  contained  a  few  drops  of  pus  in  which  there  were  some 
diplostreptococci.  The  bladder  also  was  infected  with  diplostreptococci. 
The  left  arm  was  contracted,  and  there  was  a  dry  gangrene  of  the  left 
foot. 

The  left  kidney  was  of  about  normal  size  (  I0^4  x  43./>  x  3  cm.  ),  the 
right  kidney  smaller.  The  surface  was  mottled  grey  and  red,  and  stud- 
ded with  petechial  haemorrhages.  The  renal  tissue  was  distinctly  in- 
durated, and  the  cortex  narrowed  to  about  3  mm.  Unfortunately  an 
examination  of  the  brain  and  of  the  peripheral  arteries,  and  a  thorough 
search  for  an  old  septic  focus,  was  impossible. 

Sections  showed  marked  diffuse,  subacute,  and  chronic  glomerulo- 
nephritis (intra-capillary  form),  moderate  cellular  infiltration,  and  marked 
diffuse  fibrous  thickening  of  the  connective  tissue  with  atrophy  of  many 
tubules:  much  epithelial  degeneration  and  many  casts;  blood  and  pus 
in  the  tubules,  thrombotic  hyaline  deposits  along  inside  of  walls  of  many 
arterioles,  anaemic  necroses  in  pyramids  due  to  thrombosis  of  small  arter- 
ies. Other  small  arteries  showed  marked  "endarteritis,""  and  all  the 
larger  ones  moderate  "arteriosclerosis."  \o  bacteria  were  found  in  sec- 
tions. 


Case    13.     Subacute  and   chronic  glomerulo-nephritis  in  a   child  of  8 

years  following  infectious  aneurysm  of  aorta. 
W  I.  i()0. —  \'.  I'.,  female  child,  8  years  of  age. 

The  ])atient  had  had  measles,  pertussis,  mumps,  and  chickenpox. 
There  was  no  history  of  sore  throat,  rheumatism,  or  scarlet  fever.  She 
was  apparently  perfectly  well  until  about  five  months  before  death,  when 
she  began  to  have  severe  continuous  headaches  in  the  frontal  region  with 
much  vomiting.  .About  three  weeks  later  she  had  a  "spasm"  lasting  an 
hour  and  a  half,  with  tongue  bite  and  twitching  of  muscles  of  eyes  and 
face.  This  was  repeated  six  days  later,  and  again  after  a  few  weeks. 
.\fter  the  spasms  she  was  unable  to  see  well.  The  vomiting  continued, 
and  she  developed  increased  thirst  and  polyuria.  The  |)atient  lost  much 
weight. 


Fi-.    21. 


Fig.    22 


mXORl)   OF    CASKS 


59 


Clinical  fxaniinatioii  llncc  nioiillis  luldit-  dcalii  bhuwcil  iR-iirili;.  in 
left  eye.  enlargement  of  the  liearl  with  Unu\  systolic  murmur,  |)aii)fiil 
enlargement  of  liver,  no  oedema.  Later  a  papular  eru[)tion  appeared  on 
the  extensor  surfaces  of  extremities  and  on  body.  .\  retinal  detachment 
developed  in  the  left  eye.  At  one  time  puffiness  of  the  face  was  noticed. 
She  complained  of  nnuli  pain  in  the  \nt  of  the  stomach:  nausea  and 
vomiting  continued  intermittently.  She  suffered  much  from  dvspnoea. 
and  occasionally  had  pain  in  the  region  of  the  heart,     ."^igns  developed 


of  the  jiresence  of  tluid  in  the  ])leural  cavities.  She  had  nuich  cough, 
with  blood-tinged  sputum.  Two  months  before  death,  the  arteries  in 
both  eyes  were  found  iinich  contracted,  and  there  was  marked  optic 
neuritis  and  retinitis  in  both  eyes,  iter  temperature  was  sliglitly  ele- 
vated and  irregular.  The  W'assermann  reaction  was  negative.  There 
was  a  marked  anaemia  (Mb.  60%)  and  some  leucocytosis  (28,000  grad- 
ually decreasing  to  10-12,000).  The  blood  pressure  was  about  140.  Siie 
had  a  very  marked  polyuria  all  the  time:  the  urine  was  of  low  specific 
gravity  (1002-1005).  It  contained  little  albumin  and  few  hyaline  casts, 
some  leucocytes. 


60  TIIIC    I'ATIllll.Oll'i-    OF    N'EPIIUITIS 

Necropsy  revealed  an  infectious  ( diplostreptococcic )  aneurysm  of 
the  upper  abdominal  aorta,  involving  the  orifice  of  the  left  renal  artery, 
which  was  entirely  occluded;  infarcts  in  lungs  and  spleen;  and  an  old 
tuberculous  focus  in  the  left  peribronchial  lymph-glands.  The  heart 
showed  normal  valves.  It  was  considerably  enlarged,  about  twice  nor- 
mal size,  with  marked  hypertrophy  of  the  left  and  dilatation  of  the  right 
ventricle.  The  left  forearm  and  hand  were  oedematous  on  account  of 
thrombosis  of  the  subclavian  vein.  There  was  much  chyloid  fluid  in 
both  pleurae.  The  arterioles  in  the  spleen  were  greatly  thickened  and 
hyaline.    The  other  arteries  were  normal. 

The  left  kidney  was  quite  small  (8  x  4  x  3"/^  cm.  )  with  flat  purple 
scars  at  upper  pole  and  along  the  convexity.  The  right  kidney  was  con- 
siderably swollen  ( 12  X  5  X  4J/3  cm. )  ;  the  cortex  was  wide,  yellow,  and 
opaque 

Sections  of  the  left  kidney  showed  old  focal  glomerulo-nephritis 
with  numer(3us  scars,  no  recent  processes.  Sections  of  the  right  kidney 
showed  old  glomerulo-nephritis  in  few  glomeruli  with  scar  formation 
near  them ;  hyaline  necrosis  and  subacute  glomerulo-nephritis  ( intra- 
capillary)  in  many  glomeruli ;  slight  infiltration  of  interstitial  tissue 
with  neutrophilic,  eosinophilic,  and  basophilic  leucocytes;  considerable 
proliferation  of  the  connective  tissue ;  much  granular  degeneration  of 
the  epithelium ;  many  casts,  and  leucocytes  in  some  tubules.  The  blood- 
vessels were  normal.     No  pathogenic  bacteria  were  found  in  sections. 

Case  14.     Chronic  glomerulo-nephritis  in  a  child  of  10  years  with  a 

history  of  repeated  attacks  of  tonsillitis. 
XVIII,  17. —  A.  B.,  poorly  developed  female  child,  10  years  of  age. 

The  child  had  smallpox  at  an  early  age  and  had  frequent  attacks  of 
tonsillitis.  For  the  last  two  years  she  had  had  attacks  of  precordial 
pain,  shortness  of  breath,  and  vomiting.  She  had  been  gradually  run- 
ning down  with  periods  of  exacerbation  and  remissions.  She  had  had 
transient  joint  pains  at  times.  Severe  disturbance  of  compensation 
commenced  about  two  weeks  before  death  with  oedema  involving  the 
face.  Clinical  examination  one  week  before  death  showed  a  poorly  devel- 
oped, poorly  nourished  child  with  very  marked  dyspnoea,  some  oedema 
of  the  face  but  none  elsewhere,  heavily  coated  tongue,  marked  enlarge- 
ment of  heart;  rapid,  regular  pulse  (gallop  rhythm),  no  murmurs,  en- 
largement and  tenderness  of  liver.  A  petechial  rash  appeared  on  the  skin 
about  one  week  before  death.  Towards  the  end  she  was  semi-comatose, 
verv   restless    (uraemia).      There   was    some    anaemia    (3,696,000   reds, 


I'iji.   -M- 


(>2  rin-:  i'a-i-iioi.oi;'!-  ok  mkimiritis 

111).  (So'/(  I  anil  u  sli,L;lit  k-iicocytosib  (11.400).  The  temperature  was 
suljiiormal  (about  (/r  b' )  with  rises  to  99°  and  100°  !•".  The  W  asser- 
mann  reaction  was  negative.  The  urine  (quantity  could  not  he  determ- 
inedj  showed  a  specific  gra\ity  of  about  loio,  a  heavy  cloud  ot  albumin. 
several  hyaline  casts,  and  a  tew  red  cells.  The  blood  pressure  was  lOo 
on  entrance,  but  later  fell  to  about   145. 

Xecro])s\'  revealed  a  recent  jjurulent  diplostrei)tococcic  vulvitis,  a 
congenital  fold  at  the  hiwer  end  of  the  left  ureter  with  slight  hydrone- 
l)hrosis,  ascites,  hydrothora.x,  and  slight  oedema  of  the  legs.  The  heart 
was  at  least  twice  normal  size,  with  marked  hypertrophy  of  the  left 
ventricle.  Except  for  a  few  small  yellow  spots  in  the  abdominal  aori.a, 
the  arteries  were  normal. 

The  kidnexs  had  tirmh  adherent  capsules.  They  were  small  (  lelt 
0  X  3  X  2  cm.,  right  11x4x3  cm.  ),  finely  granular,  and  the  cortex  w.as 
distinctly  narrowed. 

Sections  showed  ver\-  extensive  inxohement  of  glomeruli  ;  some 
showed  recent  hyaline  necrf)sis  of  loo])s,  others  typical  suhamite  and 
chronic  giomerulo-nephritis  ( intra-capillary  I .  There  was  a  marked 
diffuse  thickening  of  the  interstitial  tissue,  with  heavy  infiltration  with 
neutrophilic,  eosinophilic,  and  basophilic  leucocxtes :  large  areas  oi 
cicatrization  ;  blood  and  leucocytes  in  few  tubules  :  many  casts,  much 
e])ithelial  degeneration  :  marked  "endarteritis"  in  the  small,  and  mod- 
erate "arteriosclerosis"  in  the  large  arteries.  Xo  pathogenic  liacteria 
were   found  in  sections. 

Case    15.     Chronic   giomerulo-nephritis   in   boy   of  6   years   following 

streptococcic  infection  of  urinary  tract  in  nephrolithiasis. 
X\',   120. —  E.  R.,  emaciated  anaemic  boy,  6  years  of  age. 

Two  \ears  before  the  patient's  death,  a  large  stone  was  removed 
from  the  bladder.  The  urine  at  that  time  contained  pus.  The  heart 
was  clinically  normal,  hive  months  later  evidences  of  cardiac  hyper- 
trophy developed.  Later  he  had  a  right  facial  palsy.  He  had  to  urinate 
verv  frequently.  The  boy  gradually  went  down-hill,  and  eventually  died 
in  uraemic  coma.  The  history  is  incomidete,  and  there  is  no  record  of 
urinary  analysis. 

Necropsy  revealed  a  small  stone  (  1  ' ..  cm.  in  diameter)  in  right 
renal  pelvis,  with  streptococcic  infection  of  the  urinary  tract.  The  heart 
was  somewhat  enlarged,  wdth  definite  hypertrophy  of  the  left  ventricle. 
Except  for  a  few  vellow  spots  in  the  aorta  and  in  the  coronaries,  his 
arteries  were  normal. 


64 


Till-:    I'ATIKll.llliV    or    XKI'llKITIS 


The  left  kidney  sliowed  many  superficial  purple  scars,  with  narrow- 
ing- of  cortex.  In  other  places  the  cortex  was  wide  and  ojjaque.  The 
right  kidney  showed  much  more  extensive  cicatrization,  with  small  nod- 
ules of  fairly  normal  kidney  tissue. 

Sections  showed  very  e.xtensixc  chronic  glomerulo-nupliriti.'-,  with 
complete  fibrosis  of  the  [glomeruli  :  large  areas  of  cellular  iufiltraticjn,  and 


fibrosis,  with  atro])hy  of  tubules;  many  hyaline  casts  in  the  atr()|)hic 
tubules.  In  the  comparatively  normal  parts  much  recent  and  subacute 
glomerulo-nephritis  ( intra-capillary  i  :  and  a  few  granular  leucocytes  in 
the  tissues.  Blood  and  leucocytes  were  found  in  some  tubules.  Much 
granular  degeneration  and  necrosis  of  the  epithelium.  Hyaline  throm- 
bosis along  wall  in  some  small  arteries.  \'ery  marked  "endarteritis"  in 
small  and  larger  arteries,  especially  in  the  fibrous  areas.  The  sections 
were  too  badlv  contaminated  in  i)ermit  of  a  bacteriological  examination. 


RKCORl)   t  .1-    I  .\.->l„-  65 

Case  i6.     Chronic  glomerulo-nephritis  in  man  of  53  years  with  diplo- 

streptococcic  sepsis   (infected  atheromatous  ulcers  in  aorta). 
Will.  70. —  M.  K..  strongly  huilt,   fairly  wi-ll  nmnishcd  Japanese  laiin- 
dryman,  5^^  years  of  ai^e. 

(The  history  is  imperfect,  because  the  patient  did  not  speak  Knt^rjish. 
and  was  observed  for  a  few  days  onl\ .  1 

Patient  had  beri-beri  at  the  ai.;o  nf  ji,:;.  I  k-  was  a  heavy  smoker.  an<l 
he  used  much  alcohol.  For  about  the  last  three  years  his  face  and  feet 
would  become  swollen  at  intervals,  especially  when  he  drank  heavily,  and 
at  these  times  he  complained  of  distress  and  of  difficulty  in  breathins^. 
His  present  attack  started  seventeen  days  before  his  death,  with  oedema. 
Later  he  developed  a  white  membrane  in  the  throat,  which  first  appeared 
on  his  tonsils,  spreading  over  the  uvula  and  inside  of  the  cheek.  He  de- 
veloped a  high  fever,  and  had  a  very  foul  breath.  Clinical  examination 
showed  i)uffiness  of  face,  slight  oeilenia  of  legs,  angina  and  stomatitis, 
an  apparently  normal  heart.  The  pul>e  was  small,  regular,  rhytlimical, 
and  of  low  tension.  The  patient  died  with  the  signs  of  jjulmonary 
oedema.  His  urine  a  few  days  before  his  death  was  of  a  very  low 
specific  gravity  (1002),  contained  much  albumin,  occasional  granular 
casts,  and  many  white  and  red  blood  corpuscles. 

Necropsy  revealed  slight  oedema  of  conjunctivae  and  of  cheeks, 
septic  angina  and  stomatitis  (dii)lostreptococcus  infection).  In  the  lower 
thoracic  and  in  the  abdominal  aorta  there  were  large  atheromatous 
plaques,  many  of  them  ulcerated.  In  smears  from  these  ulcers  many 
diplostre])tococci  were  found.  There  was  an  old  thrombosis  of  the  left 
iliac  artery.  The  other  arteries  were  somewhat  dilated,  otherwise  nor- 
mal. The  spleen  was  of  normal  size,  and  contained  many  diplostrepto- 
cocci.  The  arterioles  in  the  sjileen  were  distinctly  thickened.  Tiie  liver 
showed  an  incipient  cyanotic  atro]ihy.  There  were  51X)  cc.  of  lluid  in 
the  ali<l(iinen.  The  i)alii-iit  died  of  broiicho-pneimionia  and  beginning 
jileuris} . 

The  lieart  was  enlarged  (one  and  one-half  times  normal  size  I.  The 
wall  of  the  left  ventricle  was  greatly  thickened  (16  mm.  in  diameter)."* 
The  heart  muscle  showed  a  marked  fatty  degeneration. 

The  kidneys  were  of  about  normal  size  (11  .v  6  x  5  cm.),  with 
granular  surface.  The  tissue  was  greyish,  with  red  blotches.  Small 
petechial  liaemorrhages  could  be  made  out  on  the  surface.  On  the  cut 
surface  the  cortex  was  found  distinctly  narrow  and  opaque.    Tiie  mucous 

■•  .Measured  from  base  of  Irabcculac  cariicac  to  outer  siirlacc. 


Fis.  29. 


Fig.  30. 


RKCORP   Ol'    I  ASIC: 


67 


membrane  of  the  renal  pelvis  and  of  the  lilaiider  was  li\  i>ei  aiTnie.  l-'ew 
diploeocci  were  found  in  smears  from  the  renal  iielvis.  1h\v  dijilococci 
were  found  in  smears  from  tlie  kidney  tissue. 

Microsco|)icaI  sections  showed  a  suliacute  and  chronic  ditfu^e  inlra- 
and  extra-cajnilary  _t;lomerulo-nei)hritis.  marked  cellular  infiltration  and 
fibrous  tliickenint;  of  the  interstitial  tissue,  with  atrophy  of  many  tubides  : 
many   neiitro|>hilic   lcucoc\tes.   much   eiiithclial    deijcneratiiin.    and    many 


Fig.  ^'■ 


ca.st>.  l)i]>lostreplococci  were  found  in  many  capillarie.--  ami  in  tlie  in- 
flamed connective  tissue  near  them :  none  were  seen  in  the  t,^lomeruIi  or 
elsewhere.  Many  arterioles  were  either  filled  or  lined  on  tiic  inside  with 
hyaline  thrombus:  sometimes  these  hyaline  masses  were  found  above, 
sometimes  underneath  the  endothelial  lining;.  In  other  arterioles  there 
was  a  marked  endarteritis,  jirobably  as  a  result  of  oru;anization  of  these 
hyaline  masses :  others  a.L^^ain  showed  a  marked  "arteriosclerosis."  The 
lars/e  arteries  showed  a  marked  "arteriosclerosis." 


68 


THK    PATIlfH.Oi 


IK    XKI'HRITIS 


Case  17.     Chronic  glomerulo-nephritis  in  man  of  48  years  with  a  his- 
tory of  scarlet  fever  and  rheumatism. 

X\  J.  2^j. —  J.  A]cL.,  fairly  well  nourished  Scotch  butcher,  48  years  old. 
Patient  had  scarlet  fever  as  a  child,  rheumatism  at  about  the  age 
of  20.  Eight  years  before  death  he  had  pleurisy.  For  the  last  two  and 
one-half  years  he  had  often  had  chills  in  the  evening  and  night  sweats; 
since  that  time  he  had  also  noticed  shortness  of  breath  and  oedema.  One 
year  before  death  he  observed  pufifiness  of  the  face.     .\t  times  he  had 


slight  pains  around  the  heart,  radiating  toward  the  arms,  lie  com- 
plained of  failing  eyesi.ght  and  frontal  bilateral  headaches.  For  these 
complaints  he  had  been  at  the  hospital  ofT  and  on,  where  a  peripheral 
arteriosclerosis,  a  cardiac  enlargement  with  systolic  and  diastolic  mur- 
murs, was  made  out,  and  a  severe  anaemia  (3,000,000  reds,  507c  lib.!. 
He  had  a  negative  W'assermann  reaction.  Eight  months  before  death 
his  blood  pressure  was  200.  .\t  his  last  entrance  it  was  210,  gradually 
falling  to  165.  Eight  months  before  his  death,  examination  of  the 
fundus  of  the  eyes  showed  an  old  disseminated  syphilitic  choroiditis,  well 
defined  arteriosclerosis,  and  evidence  of  former  optic  neuritis.     The  last 


KllKiKI)  (IK    c  ASICS  f)9 

mtiiitli  Ik-  was  more  ur  less  iinc()iiscit)iis.  at  times  liclirions  and  noisy,  and 
towards  tlic  end  had  several  uraemic  convulsions.  While  al  the  liospital 
his  temperature  and  pulse  were  normal.  lie  had  had  nycturia  (six  to 
seven  times  a  night )  for  several  years.  Mis  urine  was  greatly  increased  in 
(|uantity,  to  two  liters  and  more,  showed  a  fixed  low  specific  ijravity, 
contained  much  albumin  and  usually  many  hyaline  and  yrannlar  casts, 
and  many  leucocytes. 

.Necropsy  revealed  a  large  heart,  twice  the  size  of  the  fist ;  general 
nedema  and  hydrothorax  :  a  marked  general  arteriosclerosis,  and  almost 
complete  closure  of  the  right  coronary  artery.  The  kidneys  were  of 
ahout  normal  size,  granular. 

Sections  showed  very  marked,  difi'use  chronic  and  subacute  intra- 
capillary  glomerulo-nei)hritis.  with  unusually  extensive  hyaline  necroses 
of  the  vascular  loops:  many  large  areas  of  ccllnl.ir  infiltration,  and 
marked  diffuse  cicatrization  with  atrojihy  of  many  tubules:  few  granu- 
lar leucocytes:  casts  in  many  uibnles :  leucocytes  in  some.  'There  was 
some  fatty  degeneration  anii  necrosis  of  the  epithelium :  and  hyaline 
masses  in  many  small  arteries  causing  sometimes  complete  obstruction. 
-Marked  "endarteritis"  and  marked  ■"arteriosclerosis"  were  found  both  in 
the  small  and  in  the  large  arteries.  The  sections  were  liadh  contamin- 
ated with  colon  bacilli. 

Case    i8.     Chronic    glomerulo-nephritis    with   recent   exacerbation,  in 

man  of  45,  of  unknown  etiology. 
.\\  1.  JiJ. —  .\.  L..  well  ncjurished  Danish  male  cook,  45  years  of  age. 

rile  history  is  imperfect,  because  the  patient  entered  the  hospital  in 
a  dazed  condition  and  could  not  give  a  clear  accoimt  of  himself.  lie 
claimed  to  have  been  sufl^'ering  for  about  two  years  from  headache,  dizzi- 
ness, loss  of  memory,  failing  eyesight,  shortness  of  breath,  jirogressive 
weakness,  and  fretjuent  urination.     He  never  had  oedema. 

Clinical  examination  showed  s}mptoms  suggestive  of  partial  sensory 
aphasia,  a  marked  jjerijiheral  arteriosclerosis,  enlargement  of  heart  w^ith 
accentuation  of  second  aortic  tone,  lessened  reflexes  on  the  left  side  of 
the  body,  and  horizontal  nystagmus  to  the  left.  His  blood  w-as  normal 
excejn  for  a  slight  leucocylosis  (11.000  whites,  82'/,  nentro|>liiIes ).  The 
W'assermann  reaction  was  negative  on  repeated  tests,  both  in  blood  and 
s])inal  fluid.  His  blood-pressure  was  constantly  very  high,  varying  from 
235  to  280.  He  had  a  retinitis  albuminurica :  towards  the  end  he  had 
convulsions.  Shortly  before  death  a  petechial  rash  develoi)ed  in  the  skin 
on  hands,  chest,  and  back.    Towards  the  last  there  was  some  oedema  of 


70 


TIIR    PATMOLOCS     nV    XKI' 1 1  K  ITIS 


the  eyelids,  lie  died  in  uraemic  coma.  Mis  urine  was  increased  in  ciuan- 
tity,  pale,  clear,  of  low  specific  i;ra\ity,  and  contained  much  albumin, 
many  hyaline  and  granular  casts. 

Necropsy   revealed   a  heart   which    was   somewhat   enlar<;'ed    (about 
one  and  one-fonrth  normal  size),   with    small   scars   in  the   wall  of  the 


left  ventricle.  There  was  a  rather  well  marked  Ljeneral  arteriosclerosis 
involving'  aorta,  cerebral  and  coronary  arteries,  the  small  arteries  in 
spleen  and  pancreas,  and  manv  others. 

The  kidneys  were  small  (  ii  x  5  x  3  cm.)  and  full  of  small  haemor- 
rhages.    The  cortex  was  quite  narrow.  hy];eraemic,  and  ojiaque. 

Sections  showed  marked  diffuse  chronic  and  subacute  glomerulo- 
nephritis (intra-capillary ),  with  hyaline  necroses  in  vascular  loops;  large 
areas  of  cellular  infiltration,  and  fibrous  thickening  of  the  connective 
tissue  with  atrophy  of  tubules  :  blood  and  leucocytes  in  many  tubules  : 
much  epithelial  degeneration,  few  casts :  marked  thickening  of  intima 
both  in  small  and  in  large-arteries,  partly  with  hyperplastic  development 
of  elastic  tissue,  partly  without.  The  sections  also  showed  numerous 
small  old  necrotic  foci, — situated  near  badly  affected  glomeruli  with 
thrombotic  obstruction  of  vasa  aflferentia, — in  which  the  capillaries  w^ere 


RKCORI)  OK    CASRS  71 

liy]K'raemic,  ami  slinwcd  imicli  lilniii  in  ami  near  tlicm.  wiiitli  licranic 
hyaline  eventually.  .Many  s^ranular  lencncytcs  were  fmmd  in  and  about 
sneli  foci.  Some  of  them  showed  hei^inning'  orf>;anization.  No  bacteria 
were  tkteoted  in  .sections,  in  spile  of  esiiecially  careful  search. 


Case   ig.     Chronic  glomerulo-nephriiis   in   man  of  37   years.      No  old 

septic  focus  found,  but  a  diploslreptococcic  infection  of  the 
rectum    of    unknown    duration,    and    a    terminal(?) 
diplostreptococcic  sepsis. 
-W  1.  10. —  J.  .M..  well  nourished  Mexican  sailor.  37  years  of  age. 

I'atient  claims  to  liave  always  been  healthy  and  well,  denies  any  dis- 
eases of  childhood.  He  suffered  from  "asthma."  for  the  first  time  four 
years  before  entrance.  Two  months  before  death  he  had  achinu:  pains  in 
neck.  back,  and  extremities,  which  were  worse  at  nit^iit.  He  had  a  syphil- 
itic history  and  a  ])ositive  W'assermann  reaction.  Clinical  examination 
showed  an  enlart^cment  of  the  heart  and  a  soft  systolic  murmur,  ascites, 
proctitis,  tjeneral  oedema.  Towards  the  end  he  develoi)ed  a  marked 
dyspnoea.  There  were  no  definite  uraemic  symptonfis.  His  temperature 
showed  slijjht  occasional  rises,  and  his  pulse  varied  from  80  to  too.  His 
blood  ])ressure  was  182.  He  had  a  marked  anaemia  (2.350.000  reds: 
^o'/c  Hb.),  and  on  entrance  to  the  hospital  (two  months  before  death)  a 
Icucocytosis  (18,000),  which  disappeared  later.  I  lis  urine  contained  a 
moderate  amount  of  albumin,  few  hyaline  and  t^ranular  casts,  and  later 
many  red  cells. 

Xecrojjsy  revealed  a  muco-purulent  proctitis  due  to  (li])lostrepto- 
coccic  infection.  l"e\v  diplostreptococci  were  found  in  li\er.  spleen, 
kidneys,  and  lungs.  There  was  also  a  terminal  jiarotitis.  The  heart  was 
one  and  one-half  times  normal  size,  with  a  very  marked  concentric  hyper- 
trophy of  the  left  ventricle  (  14  mm.  1.  The  arteries,  including  the  cere- 
bral arteries,  were  normal,  except  tiie  renals,  which  showed  a  marked 
arteriosclerosis.  There  was  also  prestnt  a  general  oedema,  ascites.  h\- 
drotliorax.  and  a  cyanotic  atrophy  of  the  liver. 

The  kidneys  were  small  (  10  x  3  x  3'..  cm.),  the  surface  was  finely 
granular,  mottled  purple  and  grey.  .\'o  haemorrhages  were  seen.  The 
cortex  was  moderately  narrowed  and  opa(|ue :    the  markings  were  poor. 

Sections  showed  mostly  chronic  glomerulo-nei>hritis ;  recent  hyaline 
necroses  in  few  glomeruli :  large  areas  of  cellular  infiltration  and  cicatri- 
zation with  atrophy  of  tubules:  few  granular  leucocytes;  some  tubules 
filled  with  casts,  blood  and  leucocytes.     The  epithelium  was  tilled  with 


Fig.  35 


KKlOKU    Ol'    I  ASliS 


in^meiu   in   jilacfs  and   >lin\\i(i    nnuli    fatty   and   granular   dcijiTKTaliun. 
Ilvalini-  df|>(isits  in   llic   walls  nf  many  >niall  arlirii's,  apparently   iindt-r- 


ncatli  i'ndi]t];(.-liuni.      I'.i-^iiniini;  "endarU-ritis"  in   tht-  small  arteries  con 
nected  with  diseased  t^lomeriili,  moderate  "arteriosclerosis"  in  the 
arteries.     Xo  hacteria  were  found  in  sections. 


er 


Case  20.     Chronic  glomerulo-nephritis   in  Japanese  of  35  years  with 

old  diplostreptococcic  infection  of  tonsils. 
.Will.  1O7.— M..  stroni^ly  l.nilt.  well  nourished  iajianese  farmer.  35 
years  of  aj.^e. 
Patient  was  admitted  to  hosiiilal  live  days  hcfore  his  death,  com- 
plainintj  of  pains  all  over  body,  and  of  drowsiness.  Tiie  first  symjjtoms 
of  renal  disease  were  observed  four  years  before,  when  lie  had  y;eneral 
oedema  and  ascites,  and  was  told  that  he  iiad  kidney  disease.  Two 
months  before  death  swelling;  returned  sliijhtly,  but  disa|>iK'ared  a.L;ain  ; 
since  then  he  noticed  shortness  of  breath  and  pains  all  over  the  body. 
l""or  some  days  before  admission  he  had  headache,  and  voniite<l  several 
times.  Clinical  examination  showed  semi-stupor,  considerable  puffiness 
around  the  eyes,  heavily  coated  tontjuc  and   foul  breath,  normal  heart- 


<i:iliKn   (IF    I'ASKS 


7^ 


ilulliH'ss,  systolic  muniuir  at  liase.  accentuated  sccoiui  aortic  tone,  marktMi 
treneral  hvperaesthesia.  especiallx  of  muscles,  and  scaly  skin.  The 
temperature  was  normal.  I  lis  |)ulse  rate  was  rather  slow,  averaj^in"; 
about  64.  His  lilood-])ressure,  durintj  the  last  days  of  his  life,  was  115. 
1  le  had  a  severe  anaemia   (  2.804.000  reds :    41,'/,    Hb. )    with  poikilocy- 


tosis  and  anisocytosis  and  some  leucocytosis  (  18,000).  The  Wassermann 
reaction  was  negative  both  in  blood  and  spinal  Huid.  Towards  the  end 
the  patient  had  occasicnal  attacks  of  severe  dysjHioea,  in  one  of  which  he 
died  (uraemia).  His  urine  was  of  low  specific  gravity  (  loioi,  contained 
much  albumin,  and  in  one  specimen  many  granular  casts  and  leucocytes. 

Necropsy  revealed  chronic  tonsillitis  with  old  pus-pockets  in  crypts 
(diplostrei)tococcic  infection).  The  heart  was  about  one  and  one-half 
times  normal  size  (left  ventricle  not  dilated,  averaged  12  mm.).  The 
aorta  was  markedly  atheromatous:  the  other  arteries,  including  renals. 
were  normal. 

The  kidneys  were  small  I  9>4  x  4>4  x  3K'  cm.).  The  capsules  were 
thickened  and  adherent.  The  surface  was  somewhat  rough  and  (|uite 
])ale.  (  )n  the  cut  surface  the  cortex  was  distinctly  narrowed  ( to  2-,^ 
mm.  1  and  opaijue. 


76  Till'.    I'A'lliol.ur.v    (IF    XEI'HRITIS 

Microscopic  sections  showed  diffuse,  chronic,  intra-capillary  glom- 
erulo-nephritis,  more  subacute  lesions  in  few  glomeruh,  marked  diffuse 
fibrosis  with  large  areas  of  cellular  infiltration,  some  of  which  contain 
man)'  neutrophilic  and  basophilic  leucocytes,  marked  atrophy  of  many 
tubules,  compensatory  enlargement  of  others,  little  epithelial  degenera- 
tion, blood  and  leucocytes  in  many  tubules,  also  many  hyaline  casts, 
slight  "arteriosclerosis"  of  arterioles  in  most  fibrous  areas,  moderate 
"arteriosclerosis"  of  larger  ones.  No  bacteria  were  found  in  the  sec- 
tions, in  spite  of  careful  search. 


Case  21.     Chronic  glomerulo-nephritis  in  woman  of  36  with  old  scar 

in  base  of  aorta,  old  pericarditis,  septic  thrombosis  of  left 

auricle,  and  old  septic  infarct  in  spleen  containing 

influenza  bacilli. 

X\l,  260. —  Mrs.  K.,  emaciated  English  housewife,  36  years  of  age. 

Patient's  health  was  goofl  until  she  was  22,  when  she  had  a  severe 
infection  ("touch  of  typhoid").  Since  she  was  23  years  old,  she  had 
spells  of  intense  headache,  vomiting,  nausea,  and  occasional  nose-bleeds. 
She  had  oedema  at  times.  Eight  years  before  death,  premature  delivery 
in  eighth  month  of  pregnancy  became  necessary  on  account  of  albumin- 
uria. Before  the  birth  of  her  second  child,  two  years  later,  there  was 
much  oedema.  She  suffered  much  from  severe  dyspnoea,  pains  over 
heart  and  kidneys,  and  sleeplessness.  In  the  last  months  she  had  much 
stomatitis  and  tonsillitis.  Towards  the  end  she  was  very  weak,  rest- 
less, and  delirious  (uraemia).  The  pleurae  had  to  be  tapped  several 
times  for  hydrothorax.  She  had  a  marked  anaemia  (3,500,000  reds; 
65%  Hb. )  and  a  normal  leucocyte  count.  Her  temperature  was  normal, 
her  pulse  rate  quite  varying,  sometimes  increased  to  120  or  over.  Her 
respiration  was  about  30.  Her  blood-pressure  varied  between  160  and 
190.  She  urinated  once  at  night.  Her  urine  on  frequent  examination 
had  a  low  si)ecific  gravity  and  contained  a  heavy  cloud  of  albumin  (0.5% 
or  over ) ,  many  granular  and  hyaline  casts ;  blood  was  found  on  one  oc- 
casion. Phenolsulphone-phthalein  was  slowly  excreted  (20  resp.  11% 
first  hour,  15  resp.  21%  second  hour). 

Necropsy  revealed  an  old  scar  in  one  of  the  sinus  \'alsalvae,  a  healed 
pericarditis,  septic  thrombi  in  left  ventricle  and  left  auricle,  an  old  septic 
infarct  in  spleen  (many  influenza  bacilli  in  thrombi  and  in  infarct), 
marked  oedema  and  slight  hydrothorax.  The  heart  was  one  and  one- 
half  times  normal  size.     The  left  ventricle  measured  13  mm.,  and  was 


78 


Till-;  l^\Tllnl.()<■.^■  fii"  neimiritis 


firm.     The  renal  arteries  were  moderately  sclerosed,  the  others  jjractically 
normal. 

The  kidneys  were  small  (10x5x3  and  8>^  x  4>4  x  2>4  cm.  resp. )  : 
the  capsule  was  adherent:  the  surface  distinctly  granular;  the  cortex 
much  reduced  (to  3  mm.  in  places).     The  tissue  was  soft,  oedematous, 


Fig.  42. 


and  full  of  opaque  spots.     There  were  few  haemorrhages  in  the  cortex 
of  the  right  kidney. 

Sections  show  mostly  chronic,  but  also  some  recent,  glomerulo- 
nephritis (intra-capillary )  ;  large  areas  of  cellular  infiltration  and  fibrous 
thickening  of  the  connective  tissue  with  atrophy  of  tubules :  few  granu- 
lar leucocytes ;  little  blood  in  tubules :  granular  and  fatty  degeneration 
of  the  epithelium,  moderate  number  of  casts:  much  hyaline  underneath 
endothelium  in  several  small  arteries  :  marked  "endarteritis"  of  the  small 
arteries  and  moderate  "arteriosclerosis'"  of  the  larger  ones.  Xo  jjatho- 
genic  bacteria  were  seen  in  sections. 


KIX'IIKI)   (IF    (  ASIiS 


79 


Case  22.     Chronic  glomeriilo-nephriiis   in  man  of  42   years   with   old 
tuberculosis  and  continued  suppuration  of  the  lymph-glands 
of  the  neck. 
X\'ll.  184. —  K.  .M.,  poorly  nourished  Scotcii  clerk,  42  years  of  age. 

Patient  had  had  chronic  tuberculosis  of  lym])h-glands  of  neck  since 
childhood,  which  necessitated  twelve  operations.  I'^or  the  last  three 
years  before  entrance  he  had  had  occasional  nycturia:  for  the  past  three 
weeks  he  liad  lu-en  casiK'   fatigued,  and   siirfrred    fnini   indii/csliun  :    ;ind 


I'iH.  4X 

for  the  ])ast  ten  days  he  noticed  shortness  of  breath,  ccdema  ol  legs,  and 
oliguria.  On  clinical  examination  he  showed  a  very  marked  dyspnoea 
and  cyanosis,  very  pcjor  teeth,  slight  enlargement  of  heart,  a  soft  systolic 
murmur  at  apex,  petechiae  on  right  arm  and  left  thigh,  marked  oedema 
of  lower  extremities.  The  ])erii)heral  arteries  appeared  sclerotic.  Later 
he  develo])ed  pericardial  friction  and  signs  of  ])leurisy.  Towards  the  end 
the  patient  was  very  dyspnoeic  and  drowsy,  sometimes  delirious,  and 
showed  muscular  twitching.  Me  died  in  uraemic  coma.  Me  was  anaemic 
(3,ir)0,ooo  reds:  (12'/,  llti. »:  he  had  a  leucocytosis  (14-25,000  leiico- 
cvtes.  go';    neutroiihiles  1 .      Mis  li!oo(l-|iressiu-e  varied   from  2(X)  to  235. 


I'-iR-  45. 


RIXOKl)    OK    CASKS  81 

ilis  temperature  was  subnormal  (97  I'"),  witli  rises  to  99^  I".  His  urine 
while  at  hospital  was  scanty,  of  low  sjiecific  Ljravity,  and  contained  much 
allntmin.  many  hyaline.  e]>ithclial.  and  i^ranular  casts:  no  hlood  was 
found. 

Necropsy  revealed  numerous  old  scars  on  necU  and  slii^ht  remnants 
of  old  tubercular  infection,  recent  haemorrhaiijic  dii)lostreptococcic  peri- 
carditis and  pleurisy,  broncho-pneumonia.  The  heart  was  one  and  one- 
half  times  normal  size  (left  ventricle  averaged  14  mm.  1.  The  renal 
arteries  were  moderately  sclerosed,  the  others  [iractically  normal. 

The  kidneys  were  small  (  10  .\  4  x  _^  cm.),  the  capsule  firmly  ;iilher- 
ent.  surface  granular,  small  haemorrhages  in  cortex,  which  was  much 
reduced  (4  mm.).    The  markings  were  indefinite. 

Sections  showed  chronic  glomerulo-nephritis  in  the  majority  of  the 
glomeruli :  more  recent  changes  in  a  few :  diffuse  cicatrization  with 
small  areas  of  cellular  infiltration;  few  granular  leucocytes;  many  casts 
in  collapsed  tubules;  leucocytes  in  some  of  the  tubules;  little  cjjithelial 
degeneration  ;  hyaline  in  few  small  arteries ;  marked  "endarteritis"  in 
many  small  arteries;  marked  "arteriosclerosis"  in  few  small  and  all 
larger  arteries.     Xo  pathogenic  bacteria  were  found  in  sections. 


Case  23.     Chronic  glomerulo-nephritis  in  man  of  55  with  chronic  en- 
docarditis. 
X\  11.  iiO. —  J.  11..  well  nourished  Canadian  sailor.  55  years  of  age. 

Patient  had  repeated  attacks  of  tonsillitis,  was  in  hospital  three  years 
before  death  for  rheum.atism ;  reentered  shortly  before  death  w-ilh  acute 
rheumatism  of  hands.  There  was  no  history  of  syphilis.  The  Wasser- 
mann  reaction  was  negative.  Patient  had  "epileptic"  attacks  at  various 
times,  last  one  three  months  before  death,  lie  comi)lained  of  shortness 
ot  breath,  increasing  dimness  of  vision,  cram])s  in  legs,  and  deep  pains 
ill  bones.     I  le  never  had  any  oedema. 

Clinical  examination  showed  marked  nervousness,  hacking  cough, 
contr.uture  in  left  leg.  arteriosclerosis  of  radial  artery,  heart  within 
normal  limits,  a  soft  systolic  murmur,  no  oedema.  The  backgrounds  of 
his  eyes  showed  small,  slightly  tortuous  arteries,  otherwise  they  were 
normal.  Towards  the  end  he  had  bleeding  from  nose  and  mouth,  vom- 
ited daily,  .md  developed  uraemic  coma.  His  blood-pressure  varied  from 
190  to  2io.  lie  had  a  severe  anaemia  (2.150.000  reds;  30%  lib.  aniso- 
cytosis  ).  no  leucocytosis.  1  lis  temperature  was  subnormal.  His  ])idse  rate 
varied  between  70  and  95.    His  lu'ine  was  scanty,  of  low  specific  gravity, 


82 


TFIK    I'ATIIIII.OCN-    (IF    X  i;i' 1 1  U  ITl.'; 


C(intaiiR'(l  mucli  alluimin.  many  i^rannlar  casts,   few  leucocytes,   few  red 
cells. 

Necropsy    revealed   an   old    endocarditis   of   the   mitral    \al\'e.      Tlie 
heart    was    somewhat    enlarged.      There    was    a    terminal    hroncho-imeii- 


monia.  The  radial  artery  showed  a  marked  arteriosclerosis  :  the  cjthers 
were  much  less  involved. 

The  kidneys  were  small  and  pale :  the  capside  adherent,  surface 
granular,  cortex  narrow,  full  of  cysts. 

Sections  show  chronic  glomerulo-nephritis  in  many  glomeruli  ( intra- 
capillary),  more  recent  lesions  in  few;  very  extensive  cicatrization  of 
cortex  with  much  cellular  infiltration :  few  granular  leucocytes ;  much 
epithelial  degeneration  and  many  casts ;  leucocytes  in  few  tubules  ;  mucli 
subendothelial  hyaline  in  many  small  arteries  ;  marked  "endarteritis'"  in 
most  small  arteries,  more  "arteriosclerotic"  lesions  in  others ;  very 
marked  "arteriosclerosis"  of  larger  arteries.  No  pathogenic  bacteria 
were  found  in  sections. 


KI-UOKl)    UK    BASICS 


83 


Case  24.     Chronic  practically  healed  glomerulo-nephrilis  in  man  of  61 

with  old  history  of  rheumatism. 
X\  II,  \(>4.-     I),  (i.,  emaciated  I'rciicli  male  cnoU.  ()i  years  of  atje. 

Patient  had  rheumatism  w  lun  he  was  yoimg.  lie  denied  all  venereal 
disease.  His  present  illness  liei^an  two  years  as;o  with  loss  of  weijjfht  1  ,^5 
lbs.),  shortness  of  hreaih,  and  iiicreasinj;  weakne^s.  lie  had  to  void  his 
urine  at  night  two  to  ihree  times. 

Clinical  examination  showed  a  marked  puffiness  of  skin  about  eyes, 
much  dyspnoea,  coated  tonnne.  and  fmil  breath,  enlarged  heart,  a  rough 


.-^^S^liv^^i 


systolic  and  faint  diastolic  murmur  o\er  the  heart.  'I'lie  rhythm  of  the 
heart  was  absolulel\  irregular.  Mi--  li\ei-  was  enlarged.  His  blood- 
pressure  on  entrance  was  170.  later  u;ra<luall\  went  down  to  137.  I'atient 
had  no  marked  oedema  at  any  time,  lie  had  a  severe  anaemia  (3.500,- 
000  reds  and  4S' ;  lib.  1.  also  a  slight  leueoeytosis  (  I4,C)(X)).  The  VV'as- 
sermann  reaction  was  negative.  The  urine  was  scanty  at  first,  later 
about  normal  in  (|uautity.  The  specilie  gravity  was  about  loio.  It 
contained  e(jnsiderable  .albiunin.  ami  at  times  many  granular  casts  and 
red  cells.  The  patient  at  no  time  showed  detinite  symptoms  of  uraemia. 
lie  died  with  the  clinical  symptom>  of  an  acute  i)ulmonary  infection. 


84 


THK    l'ATll()|.(li;V    OF    NKI'Il  RITIS 


Necropsy  revealed  marked  general  arteriosclerosis,  a  very  marked 
enlargement  of  the  heart  (about  three  times  normal  size),  small  scars 
in  heart  muscle,  gouty  deposits  in  kidneys  and  toe  joints,  a  terminal 
broncho-pneumonia,  beginning  cyanotic  atrojihy  of  liver. 

The  kidneys  were  small  (  lo'/j  .\  4  x  4  cm. )  :  the  capsule  stripped 
easily.  The  surface  was  coarsely  granular.  The  cortex  was  much  re- 
duced, and  the  markings  were  very  indistinct. 

Sections  show  chronic  glomerulo-nephritis  in  many  glomeruli  with 
large  areas  of  cicatrization  in  cortex,  comparatively  little  cellular  infiltra- 
tion, few  granular  leucocytes  :  subacute  glomerulo-nephritis  ( intra-cap- 
illary )  in  few  glomeruli ;  leucocytes  in  few  tubules  ;  little  epithelial  de- 
generation ;  very  marked  "arteriosclerosis"  of  large  and  small  arteries. 
Xo  bacteria  were  found  in  sections. 

Case  25.    Chronic  glomerulo-nephritis,  in  man  of  60  years,  of  unknown 

etiology. 
XVni,  108. —  T.  H.  D.,  poorly  nourished  man,  60  years  of  age. 

No  history  could  be  obtained  on  account  of  the  condition  of   the 


patient.    Patient  entered  the  hospital  in  a  delirious  condition.    He  showed 
a  coarse  tremor  of  the  extremities,  a  jerking  of  the  head,  and  consider- 


Uli  liKli    111-     I  ASKS  85 

alilt,-  ri^itlity  of  tlic  m-ck.  Tlu-  rt-lloxes  were  exaggeratetl.  Tliere  was  an 
infected  wduiul  (i\er  the  iicri|nit.  I  lis  tem])eratiire  ranj^ed  between  9//)° 
and  yy.5  i'.  J  lis  pulse  was  Jiiiili  and  irregular.  He  had  no  oedema,  lie 
died  three  days  later  in  coma. 

Necropsy  revealed  a  hejjinninj^  ])rostatic  hypertrophy  and  terminal 
hroncho-pneumonia.  His  heart  was  of  normal  size.  There  was  a  slight 
concentric  hypertrophy  of  the  left  \entricle.  .\11  arteries,  the  aorta  and 
cerebral  vessels  included,  showed  a  marked  arteriosclerosis. 

The  kidneys  were  small  t').~  .\  4  \  J.^i.  The  capsule  stripped  with 
dil'licnJiy.  The  surface  was  granular.  Tlie  cortex  was  narrow  and 
opa<|ue.     There  were  no  \isilile  JiaemorrhaLjes. 

.Microscopical  sections  sjiowcd  very  extensive  (jld  i^lonierulo-nephritis 
of  many  glomeruli,  much  cellular  infiltration  and  fibrous  ihickeninjj;  of 
tlie  connective  tissue  with  atro])hy  of  L^roujis  of  tubules,  much  epithelial 
detjeneration.  many  casts  and  leucoc\tes  in  tubules,  considerable  \n<^- 
mentation  of  the  epitliehinii.  'i'lie  arterioles  and  llic  lari.;er  arteries 
sliowed  a   \er\-  marked  "arteridsclerdsis." 

Case  26.    Chronic  glomerulo-nephritis,  in  man  of  54  years,  of  unknown 

etiology. 
Will,  ly. —  S.  G.,  emaciated  Irish  teamster,  54  years  of  age. 

I'atient  did  not  recall  any  diseases  except  measles  in  infancy.  He 
was  a  heavy  beer  drinker.  He  had  gonorrhoea  at  35,  denied  lues.  Five 
years  before  death  he  became  dropsical  for  the  first  time ;  he  had  another 
attack  one  year  ago,  associated  witli  "rheumatism."  He  comjilained  of 
dropsy,  shortness  of  breath,  |ial|iitaIions.  and  jirecordial  pain,  heailache, 
and  [jains  in  legs. 

t'jinical  examination  showed  marked  drowsiness,  marked  oedema  of 
face,  coated  tongue,  poor  conditiim  of  few  lemaining  teeth,  enlargement 
of  heart,  distant  heart  scninds  but  no  definite  murmurs,  ascites,  general 
oedema.  Towards  the  end  he  became  delirious,  and  died  in  uraemic 
coma,  llis  blood-pressiu'e  \aried  between  icjo  and  210.  He  had  some 
anaemia  178';  Mb.  1.  no  leucocytosis.  llis  temperature  was  normal  and 
at  times  subnormal,  llis  pulse  rate  varied  between  80  and  130.  His 
urinary  output  \aried  between  1400  and  2500  ccm.  daily.  The  s])ecific 
gravity  was  low.  Tlie  urine  contained  a  heavy  cloud  of  albumin,  occas- 
ional hyaline  casts,  few  leuc<)C\tes.  no  blood.  There  was  practically  no 
excretion  of  i)henolsul])hone-i)hthalein. 

Xecrojisv  revealed  a  slightly  enlarged  heart  (  left  \entricle  avera.ged 
I J  mm.  I.  marked  arteriosclerosis  of  coronaries  and  of  all  abdominal 
.arteries,  c\anotic  atrojibv  of  the  liver,  much  oedema,  ascites  and  hydro- 


86 


THK    I'ATIIOl.OCY    ()!••    N'EI'IIRITIS 


thorax,  recent  haemorrha,t,MC  iiericarditis  without  bacterial  finding-.s.  He 
also  had  f^outy  joints. 

The  kidneys  were  small  ( 8>2  x  3,!-..  x  3  cm.  1  :  the  capsule  was  thick 
and  adherent :  the  surface  granular.  The  corte.x  was  much  reduced  (to 
about  3  mm.  1  and  full  of  c}sts  ;    the  markings  were  poor. 

Sections  showed  chronic  glomerulo-nephritis  in  man}-  anrl  subacute 
lesions  in   few  glcmeruli  ;    large  areas  of  cellular  infiltration  and  fibrous 


thickening  of  the  connective  tissue  with  atro])hy  of  the  tubules  ;  moderate 
infiltration  with  neutrojihilic  leucocytes,  few  eosinophiles  and  basophiles  ; 
slight  epithelial  degeneration,  many  casts  in  atrophic  tubules :  subendothe- 
lial  hyaline  in  few  small  arteries :  marked  "arteriosclerosis"  and  "en- 
darteritis" in  small  arteries,  marked  "arteriosclerosis"  in  large  arteries. 
No  bacteria  were  found  in  sections. 

Case  27.     Chronic  glomerulo-nephritis  in  man  with  old  "malaria"  and 

terminal  septic  lesions. 
X\'II,  82. —  C.  S..  well  nourished  .\merican  male  nurse,  31  years  of  age. 
The  history  is  imperfect.     "He  had  "malaria"  two  and  one-half  years 
ago  which  was  recurrent."     He  had  syphilis  at  the  age  of  26,  and  sev- 
eral attacks  of  gonorrhoea. 


OS  Till-:    IV\TII(i|.n(i\-    III"    NKI'IIRITIS 

Necrop.sy  rc-\calcd  an  ulctralivu  diplcjstreptococcic  stomatitis,  an 
acute  suppurative  pericarditis  without  bacterial  findings,  and  an  acute 
endocarditis  of  the  mitral  valve.  'J'he  heart  was  one  and  one-fourth 
times  normal  size,  and  the  left  ventricle  averaged  15  mm.  There  was  a 
marked  arteriosclerosis  of  the  aorta,  coronaries,  splenic,  renal,  and  cere- 


bral arteries.  The  liver  showed  cyanotic  atrophy  with  compensatory 
hypertrophy  of  the  peripheral  parts  of  the  lobules. 

The  kidneys  were  small  (8^4  x  4  x  3  cm.)  and  granular,  showing 
grey  spots  on  a  red  background.  There  were  many  haemorrhages  in 
the  cortex.  The  latter  was  nuich  reduced.  Some  gouty  deposits  were 
found  in  the  pyramids. 

Sections  showed  chronic  glomerulo-nephritis  of  most  glomeruli  and 
more  subacute  lesions  (intra-capillary )  in  a  few;  almost  total  destruc- 
tion of  the  cortex  by  fibrosis,  much  cellular  infiltration ;  few  granular 
leucocytes ;  blood  and  leucocytes  in  many  tubules,  much  epithelial  degen- 
eration, many  casts :  "endarteritis"  in  few  small  arteries,  very  marked 
"arteriosclerosis"  in  the  rest.     No  bacteria  were  found  in  sections. 


Ki;C()Kl>   OK    CASKS 


89 


Case  28.     Chronic  glomerulo-nephritis  in  man  of  24  years  with  chronic 

endocarditis. 
W'll.  149. —  L.  A.,  well  noiirislied  Italian  hoxniakc-r,  24  years  i)f  a^e. 

The  patient's  general  health  had  heen  good  until  one  year  he  fore  his 
death,  when  he  had  rheumatism  in  feet  and  hands.  His  present  illness 
started  four  months  ago  with  ejiistaxis.  shortness  of  hreatii  and  jiain  in 
the  epigastrium. 

Clinical  examination  showed  continued  iiieeding  from  nasal  mucous 
membrane,  a  heavily  coated  tongue.  \ery  marked  dyspnoea  in  si)ite  of 
comparatively  little  circulatory  disturhance   (  m'aeniic  air  hunger  1.  mod- 


erate dilatation  of  the  heart  towards  the  right,  a  i)resystolic  murmur,  nor- 
mal rate  and  rhythm  of  heart  beat.  Patient  had  no  oedema  at  any  time. 
He  had  a  severe  anaemia  (3,100.000  reds:  48'^  lib.  >  :  towards  the  end 
much  leucocytosis  (39,600;  c;3^r  neutrophiles ).  llNind  culture  was  nega- 
tive. His  temperature  was  subnormal.  I'^or  the  last  one  and  one-half 
months  he  voided  urine  four  to  five  times  at  night.  It  was  <if  low 
s]>ecific  gravity  (loii)  and  contained  much  albumin:  no  casts.  ( (Jne 
examination,  as  patient  was  in  hosj)ital  one  day  only.  I     No  coma. 


tig.  54- 


I'lg^  55. 


RKlOKI)   OK    lASKS  91 

Xfcro]isy  revcali'<i  an  did  cnilncarclitis  of  tlif  mitral  \al\i-  with  iinid- 
t-rate  stenosis  (no  bacteria  loundi.  recent  ai)|)arently  emliolic  imstiilcs  on 
chin  and  left  liand.  a  heart  of  normal  size  on  tlie  left,  slight  dilatation 
on  the  rii,dit  side;  an  old  primary  tnbercidosis  of  the  intestines  and  of 
tile  mesenteric  lymi)h-_t;:lan(ls.     The  arteries  were  normal. 

'VUe  kidneys  were  small  (9J/2  x  4>4  x  3  and  7  x  4  x  2'/^  cm.,  res])ec- 
tivel\  I.  I'he  ca]isiile  was  adherent:  snrface  coarsely  ijranular,  cortex 
very  narrow,  o[)a(|ue,  very  liijht  in  color,  almcjst  yellow. 

Sections  show  chronic  £;lomeriilo-ne])hritis  in  many  glomeruli,  more 
recent  changes  ( intra-ca|)illary )  in  few;  large  areas  of  fibrosis  with 
atrophy  of  tubules:  few  areas  of  cellular  inl'iltration  :  considerable  num- 
ber of  eosinophiles.  fewer  ueutrophiles  and  basophiles;  many  casts,  few 
leucocytes  in  some  liiimles:  little  ei)ithelial  degeneration:  marked  "en- 
darteritis" of  small  arteries,  slight  "arteriosclerosis"  of  the  larger  ones. 
Xo  bacteria  were  found  in  sections. 


Case  29.     Chronic  glomerulo-nephritis  in  man  of  59  years  with  pos- 
sibly old  septic  focus  in  urinary  tract. 
.\\  1.  iH'). —  S.  (i..  emaciated  Chinese  male  cook.  59  years  of  age. 

The  history  is  incomplete,  because  patient  did  not  speak  English, 
lie  had  noticefi  puffiness  of  the  face,  shortness  of  iireath.  paljiitation  and 
pain  over  heart,  and  swollen  legs  for  the  last  four  to  live  months.  He 
vomited  occasionally,  liut  had  no  headaches.  Clinical  examination 
showed  poor  teeth,  a  normal  heart,  and  oedema  of  the  lower  extremities, 
lie  had  a  \ery  marked  anaemia  (2,iC)o,cxx)  reds:  35'/?  111).),  no  leuco- 
cytosis.  I  lis  temi)eratnre  was  subnormal.  His  pidse  rate  varied  between 
60  and  80.  The  urine  (one  examination)  contained  a  moderate  amount 
of  albumin,  no  casts,  many  epithelial  cells,  and  few  leucocytes. 

.Xecropsy  revealed  a  small  heart,  normal  arteries  excejjt  some  ather- 
f)ma  of  the  aorta  and  moderate  arteriosclerosis  of  the  renal  arteries, 
beginning  cyanotic  atrophy  of  liver,  general  oedema,  marked  ascites  and 
Indrothorax :  gouty  deposits  in  ears,  basal  joints  of  great  toes,  and  kid- 
neys :   i)urulent  cystitis  and  prostatitis. 

The  kidneys  were  very  small  (S  x  3>4  x  2]/:  and  7  x  3'-<  x  2'/;  cm., 
respectively)  :  the  capsule  was  adherent,  the  surface  granular,  the  cortex 
very  narrow  {2-^  mm.). 

Sections  showed  chronic  glomerulo-nephritis  of  most  glomeruli, 
more  sub-acute  lesions  ( intra-capillary )  in  others,  considerable  hyaline 
necrosis   in   affected   glomeruli  :     very   extensive    cicatrization   of   cortex 


i<"ig-   57. 


Ki:a)KI>   OK    I  ASK: 


93 


with  some  ureas  of  cellular  infiltration;    very  few  tjranular  leucocytes; 
inticli  epithelial  defeneration;    very  many  casts,  hinod  in  some  tuhules; 


very  marked  ''arteriosclerosis"  of  the  small  arteries,  less  in  the  lartje  ones. 
Xo  pathos;;enic  bacteria  were  found  in  sections. 


Case  30.     Chronic  glomerulo-nephritis  in  man  38  years  of  age  with 
a  history  of  repeated  attacks  of  tonsillitis. 
.\\  .  ,^,V —  I.  C'..  stronsjly  liuilt  l)oilermaker  and  bartender.  38  years  old. 

Patient  had  been  subject  to  strain  and  bad  weather  for  twenty-five 
years,  lie  had  frequent  attacks  of  sore  throat  and  many  colds.  lie  li.id 
used  alcohol  to  c.xcess.  lie  had  ijonorrhoea  and  chancroid  at  24.  When 
he  was  30  he  had  an  attack  of  "rheumatism"  in  the  risjlit  great  toe; 
about  one  year  before  his  death  he  had  "rhciunatism"  in  .several  joints 
and  facial  palsy  following  i)ain  at  base  of  skull.  Clinical  examinatinn 
showed  marked  anaemia,  coated  tongue,  bad  teeth,  heart  within  normal 
limits,  no  murmurs.  No  oedema.  At  the  hospital  he  had  a  fit  of  "epi- 
lepsy." lie  had  a  suspicious  Wassermann  reaction.  His  blood-|)ressurc 
was  iTio.     He  had  a  severe  anaemia  (2.700,000  reds;    .^3%  HI),  no  leucn- 


94 


•IHI-;  l'.\Tll()l,()l;^    (ii--  .\i:i'i iritis 


cytosis).  His  temperature  was  .slij;htly  sulmormal.  Ills  pulse  rate 
varied  from  84  to  too.  The  last  three  days  he  had  coiUiiiued  epistaxis. 
He  had  to  void  urine  fre(|uently  and  to  get  up  several  times  at  nii^ht. 
L'rinanalysis  (one  examination)  showed  specific  gravity  of  1023,  no 
albumin,  few  granular  casts,  leucocytes  and  erythrocytes. 

Necropsy    revealed     purulent    bronchitis    and    broncho-pneumonia. 
haem(jrrhagic  pleurisy  and  pericarditis.     The  heart  was  slightly  enlarged 


I'iy.   .SQ. 


I  left  ventricle  averaged  12  mm.).  The  blood-vessels  were  practically 
normal.     There  were  gouty  deposits  in  toe  joints  and  kidneys. 

The  kidneys  were  small  (9/^  x  4  x  2J/2  cm.)  and  granular.  The 
cortex  was  much  reduced,  and  the  markings  were  indefinite. 

Sections  show  chronic  glomerulo-nephritis  in  the  majority  of  the 
glomeruli,  more  subacute  lesions  (intra-capillary  )  in  the  few  remaining 
ones,  very  marked  dififuse  cicatrization  of  cortex — with  little  cellular  in- 
filtration :  few  small,  fairly  intact  areas  of  kidney  tissue ;  much  epithelial 
degeneration,  many  small  epithelial  cysts;  blood  and  leucocytes  in  few- 
tubules  ;  hyaline  masses  in  few  small  arteries ;  marked  "arteriosclerosis" 
of  many  arterioles ;   moderate  "arteriosclerosis"  in  larger  arteries. 


RKl(lKl)   OF    (.ASKS 


95 


Case  31.     Chronic  glomerulo-nephritis  in  woman  of  28  years  with  old 
ulcer  of  tonsil  and  chronic  diplostreptococcic  infection 
of   urinary  tract. 
X\  11.  ()8. —  Mrs.  Li.  li.,  emaciated  .\mcricaii  domestic,  J8  year.s  of  age. 
I'atient  had  always  been  in  poor  health:   had  "La  (jrippe"  as  a  girl; 
iiad  liad  chronic  catarrh  for  many  years.     Nine  years  before  death  ap- 
pendectomy   was    performed    for    acute    ai)])endicitis.      She    had    kidney 


I'it;.   (n 


trouble  while  carrying  her  first  child,  live  years  before  death,  again  when 
carrying  the  second.  About  one  year  before  death  she  noticed  pro- 
gressive debility  with  anorexia  and  vomiting.  A  little  later  she  had  some 
attacks  of  violent  delirium  with  comi)lete  unconsciousness.  She  voided 
much  ])ale  urine.  For  the  last  seven  months  she  had  headache,  vomiting, 
jerking  and  cramjjs  in  legs,  palpitations  of  the  heart,  progressive  weak- 
ness and  loss  of  weight.  i>n)gressive  amaurosis,  and  at  times  oedema  of 
the  feet ;   towards  the  end  jjatient  was  very  noisy,  restless,  and  delirious. 


FiK.  6i. 


Mg.    6. 


Kit  111(11    (II-    CASKS  97 

llcr  ton,mic  was  heavily  coated  and  lur  luealli  uiainiic.  I  icr  tfm|KT- 
atiire  was  normal,  her  pulse  varied  i^reatly  (l)etweeii  So  and  uoi. 
Ophthalmoscopic  examination  showed  an  albiiniinnric  retinitis.  Her 
hiood-])ressiire  was  185.  She  died  in  uraemic  coma.  She  had  a  marked 
anaemia  {2,700.000  reds;  40';}  Hb.),  some  lencocvtosis  (14.000),  867^, 
nentrophiles.  The  W'assermann  reaction  was  netjalive.  The  phenolsnl- 
phone-phthalein  excretion  was  diminished  (i.  hour  5'/;  ;  2.  hour  25%  I. 
The  urine  was  increased  in  (|nantity.  nf  Inw  si)ecific  gravity  (  loio  or 
less),  contained  much  alliuniiii  (tn  _>' ,  1,  occasional  showers  of  casts, 
few  red  cells,  and  few  leucocytes. 

Necropsy  revealed  a  heart  aliout  one  and  une-hall  tinu>  normal  size 
I  left  ventricle  averatjed  about  11  mm.),  normal  blood-vessels,  an  old 
ulcer  of  the  tonsil,  chronic  diplostreptococcic  cystitis  and  i>yelitis  ( diplo- 
streptococci  also  found  in  risjht  kidney  1.  liaeniorrhaLjic  tlnid  in  both 
pleurae  and  terminal  broncho-pneumonia. 

The  kidneys  w'ere  very  small,  cspeciall\'  in  aniercj-posterior  diameter 
(9x4x3  cm.),  coarsely  granular,  full  of  lar<;e  retracted  scars:  the 
cortex  was  very  narrow  and  full  of  opaque  spots. 

Sections  showed  mostly  chronic  ^[^lomerulo-neijliiitis.  more  recent 
lesions  in  few  t^lomeruli  (intra-capillary )  ;  large  areas  of  cicatrization 
with  much  cellular  infiltration  :  few  granular  leucocytes ;  moderate  epi- 
thelial degeneration :  many  casts,  blood  and  leucocytes  in  some  tubules : 
marked  "arteriosclerosis"  of  small,  less  so  of  large  arteries.  No  Ijacteria 
were   found  in  >cctions. 


Case   32.      Chronic   glomerulo-nephritis  in  man  of  24  years   with   in- 
definite septic  history. 
X\'.  <>/. —  (i.  .\.,  emaciated  Canadian  jockey,  24  years  of  age. 

History  imperfect.  Patient  when  a  boy  had  "malaria"  several  times, 
a  definite  attack  of  rheumatism  one  year  before  death.  When  n;  he  had 
a  chancre  without  secondaries,  lie  had  been  losing  weight,  had  fre(|uent 
nose-bleed,  and  was  markedly  anaemic.     His  tem])erature  was  subnormal. 

Necropsy  revealed  a  rather  small  heart,  normal  blood-vessels,  slight 
ascites,  more  marked  hydrothorax,  no  subcutaneous  oedema,  and  terminal 
lironcho-pneumonia. 

The  kidneys  were  very  small  ( 8J4  x  3><  x  2  and  7J/2  x  3>^  x  3  cm., 
respectively)  :  the  cajisule  was  firmly  adherent;  the  corte.s  was  thin  and 
opaque,  and  full  of  yellow  sjxits. 


Fig.  6,v 


Fig.  64. 


UKlOKIi   (IF   lASi;s  'W 

Sections  sliowcci  clironii-  i;l()iiu-nilc)-iu-|iliTiiis  of  piairtically  all  glom- 
eruli,— much  hyaline  in  the  affccled  s^iunieruii ;  almost  complete  destruc- 
tion of  cortex  by  cicatrization,  many  lari;e  areas  of  cellular  inliltration ; 
much  epithelial  degeneration,  moderate  numher  of  casts,  blood,  ancl 
leucocytes  in  some  tubules ;  moderate  "endarteritis"  and  "arteriosclerosis" 
in  small  \essels,  slight  "arteriosclerosis"  in  large  ones.  The  sections 
were  too  badly  contaminated  to  ])ermii  of  bacteriological  examination. 


SUMMARY    OF   CASE 


Sex  and 
Age 


Etiology 


Condition  of  Kidney 


I.  xvii,    60        M,5J 


2.  XVII,    31 

3.  xvii.  188 

4.  xviii,  158 


Mo4 
M.4I 
F,  33 


Diplostreptococcic 

endocarditis. 
Diplostreptococcic 

endocarditis. 
Diplostreptococcic 

endocarditis. 
Streptococcic 

ulcers  of  legs. 


Swollen,   opaque,    few   haemorrhage! 

6x3) 
Xormal  size,  many  haemorrhages 

Much    swollen,    opaque,    few    haemo 

(13x7x4;/;) 
Distinctly  swollen,  hv|ieracmic,  oede 

(12^^x6x4/2) 


11.  SUBy^ 


5- 

xviii, 

166 

F, 

33 

Diplostreptococcic 
endocarditis. 

Swollen,  many  Iiaemorrhages   (I2x 

6. 

xvi. 

56 

F,2 

nio. 

Colon  bacillus 
pyelitis. 

Swollen,  opaque 

7. 

xvii. 

163 

M 

40 

Diplostreptococcic 
endocarditis. 

Swollen;  cortex  wide,  opaque,  m.mj 
orrhages 

8. 

xiv. 

34 

M 

4.T 

Streptococcic 
infection. 

Swollen,  opaque,  mottled,  many  1 
rhages    (12x7x4) 

9- 

XV, 

135 

M 

33 

Diplostreptococcic 
endocarditis. 

Xormal  size,  cortex  wide,  opaque 
haemorrhages 

10. 

xviii. 

106 

F. 

-7 

Abscess  of  jaw. 

Xormal   size,   cortex    wide,   yellow, 

1 1 

xvii. 

119 

M 

51 

Diplostreptococcic 
endocarditis. 

Swollen,  many  haemorrhages,  cortex 

ij. 

x\iii. 

61 

F. 

26 

Tonsillitis 

Slightly  reduced  in  size,  many  1 
rhages   (  io"4  x  4'S  x  3) 

III.  SUBACUTE  AND  CHR 


i^.    xvi,  190 

F,  8 

Infectious     aneu- 

Rt. kidnev  swollen,  pale,  opaque ;    U 

rysm,  diplostrep- 

traded  (8  x  4  x  3'<) 

tococcic. 

14.   xvii,    17 

F,    ID 

Tonsillitis. 

Small,  granular  (6x3x2;  9  x  4  x  3 
tex  narrow 

15.        XV,  120 

M,  6 

Streptococcic   cys- 
titis  :ind   pyelitis. 

Small,  with   large  deep   scars 

,ERULO-NEPHRITIS 

;rl'lo  \i;i'iiKiTis 


idilion  of  Urine 

Hypertension  and 
Cardiac  Hypertrophy 

Arterioscle- 
rosis, Local 
and  General 

Oedema  Uraemia 

Retinitis 
albu- 
min- 
uricB 

Anae- 
mia 

r,M,   Erylhro-  Leuco- 
'''^'^  [  cytes  1  cytes 

.^. 

-         - 

_ 

I0C.+ 
gen.+ 

card. 

- 

- 

+ 

_         _ 

— 

1    I0C.+ 

card. 

_ 

_ 

■H 

■   gen.+ 

—         — 

— 

I0C.+ 
gen- 

4+ 

— 

— 

> 

■HH-     1       —           4-H 

— 

I0C.+ 
gen.- 

+ 

— 

— 

« 

■Il'LO  XICPllRITl 

s 

+++ 

+++       +++ 

- 

loc- 
gen.- 

+ 

+ 

- 

++ 

—         — 

— 

loc- 
gen.- 

+ 

— 

— 

— 

~         — 

— 

loc- 
gen.- 

+ 

— 

— 

+ 

SI.    livi)ort.    of   left 

I0C.+ 

+ 

— 

— 

■H- 

ventricle? 

geii.+ 

■\-^        ++ 

" 

loc- 
gen.- 

4- 

— 

— 

++ 

-H+ 

++        ++ 

I?. I'.   170;  11.  si.  h. 

I0C.+ 
gen.- 

++ 

— 

+++ 

++     ,       -H- 

H.  F.  -'00 ;    H.  2x 

I0C.+ 
gcn.+ 

+ 

— 

— 

-H- 

+++ 

4+             ++ 

H.    I'.    180:     11.  n. 

loC.-H- 

gcn.-H 

+-+ 

^ 

( 

4-(- 

^ULO-NI£PHRITI 

S   IN"   CHILDREN'. 

+ 

— 

P.     I'    140:    H.  2x 

loc- 
gen.- 

- 

+ 

+ 

+           — 

H.    1'    150:    H.   2x 
11     hyp    Irft 

I0C.+4 
gcn.- 

1 

IV,  cm 


Case  No. 

Sex  and 
Age 

Eliolooy 

Condition  of  Kidney 

l6.  xviii,  170 

M.S3 

Diplostreptococ- 

Normal     size,     slightly    granular,    r 

cus  sepsis. 

some  haemorrhages 

17.    xvi,257 

M.48 

Rheumatism. 

Normal  size,  granular 

18.    xvi.  212 

M.45 

(  ?)   History  imperf. 

Small     (11x5.x  3).     many     haenior 
cortex   narrow 

19.    xvi,    10 

M,37 

Diplostreptococ- 

Small    (lOxSy-S'A),  mottled;   cort 

cus   sepsis  (  ?). 

row,  opaque 

20,  xviii,  167 

M,3S 

Tonsillitis. 

Small    (9>^x4!/i  x3!^),  pale;    cort 
row,  opaque 

21.     xvi,  260 

F,  36 

Old  infection   with 

Small   (9x5x3),  granular,  cortex 

influenza-bacilli 

opaque,  few  haemorrhages 

22.  xvii,  184 

M,42 

Chronic    tuberculo- 

Small   {10x4x3),   granular;     cortt 

sis   and   suppura- 

row, few  haemorrhages 

tion   of  glands 

23.   xvii.  1 16 

M,5S 

Old   endocarditis 

Small,  pale,  granular;  cortex  narrow 

24.   xvii.  164 

M,6i 

RlicuTuatism 

Small   ( io.'/l>  X  4  X  4) ,  granular  ;  cort 
narrow- 

25.  xviii,  108 

M,6o 

(  ?)   \o  history 

Small   ( 10  X  4  X  2'/,),  granular  ;  cort 
row,  opaque 

26.  xviii.    19 

M,54 

(?) 

Small     (8i4x3!^x3),     granul.ir; 
narrow,  cystic 

27.  xvii,    82 

M,3i 

(  ?  )   History  imperf. 

Small   (8'<ix4x3),  granular;  many 
orrhages 

28.  xvii,  149 

M,24 

Old   endocarditis 

Small   (8x4x3),  granular;  cortex 
pale 

29.    xvi,  189 

M,59 

(  ?)   History  imperf. 

Small    (8x3x25^),  granular;    cort 
narrow 

30.     XV,    33 

M,38 

Tonsillitis 

Small     (9^/2x4x2;/^),     granular; 
very  narrow 

31.  xvii,    68 

F,  28 

Tonsillitis 

Small     (9x4x3),    granular;    corte 
narrow 

32.     XV,    97 

M,24 

Old  sepsis  suspected 

Small      (S'/zx  3'A  x2).     granular; 
very  narrow 

Key  to  abbicviations :     M,  male  ;      I*",   female  ;      P,  polyuria ;      B.   P.,  blood-p 
+-H-,  marked ;     — ,  negative ;  ?,  unknown   or  questionable.     All   measui 


•.RLU)-.\l-:i'llKI  I  IS 


edition  of  Urine 

c«ts  ^'!^'°- 

I  cytes 


Hypertension  and 
Leuco-       Cardiac  Hypertrophy 
cytes 


Arleriosclc- 

rosis,  Local  lOedema  Uraemia 

and  General 


Retinitis 
albu-     Anae- 
min-    I    mia 
urica 


+    !       ++            -H- 

1      1 

(?)    11.    iKx 

loc.-H-                 1  ' 

gcn.-f 

- 

B.P.  joo:     H.   2x 

loc.H- 
sen.-H- 

? 

—        — 

B.P.  .'50 :   H.   i''4X 

loc.-t^+ 
;.  en.-H- 

•f 

— 

R.P.   i8.':  H.   iVSx 

loc.-r-i- 
gen.- 

— 

li.r    115;   H.  i'Ak 

loC.-r 

gen.- 

— 

W.V.   180;   M.   i''2X 

loc.-H- 

gCMl.- 

— 

l!.P.  230;   n.    I'/'X 

loc.-H                    H 
gcn.- 

■f 

— 

R.P.  200:   H.   I'ix 

loc.(-f!              — 

iicn.i 

+ 

— 

R.P,   170:   H.  .?x 

lor.-i4-              -I 
gen  .+-H- 

— 

— 

R.P.    (?):    H.    n. 

loc.-t-H-          — 
gcn.-H-+ 

+ 

— 

R.P.  200:   II.   i'/4X 

loc.-H-f             + 
gen.-H-l- 

+ 

— 

B.P.   (  ?)  ;   H.  i'4x 

loc.-H-H              ? 
geii.-H- 

5 

— 

B.P.    (?);     H.   n. 

Ioc.4-f             — 
gen.- 

— 

— 

I'..P.    (  ?)  :    H.   sm. 

loc.-H-i-             -H 
gcn.-h 

+  ? 

— 

R.P.   160;   11.  i^x 

10C.-H4      i     — 
gcn.- 

^- 

— 

R.P.   1S5:   H.  iV^x 

loc.H               -1 
gcn.- 

•H- 

■h 

R.P.    (  ?)  :    11.   sm. 

I0C.+         '        + 
Bcn.- 

> 

— 

^'cncral  ;       c.-irfl.  cardiac.       i.   slight;      4-f.   inodcrato ; 


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